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Hypertension in Dahl salt-sensitive rats: biochemical and immunohistochemical studies.
1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques. 2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats. 3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets. 4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different. 5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet. 6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.
Angiotensin II↗
Salt intake and plasma atrial natriuretic peptide and nitric oxide in hypertension.
In response to a high salt intake, salt-sensitive hypertensive individuals retain more sodium and manifest a rise in blood pressure greater than that in salt-resistant individuals. In this study, we tested whether salt sensitivity might be related at least in part to reduced secretion of atrial natriuretic peptide (ANP) or to abnormal nitric oxide production. We measured plasma ANP and NO2+NO3 in 7 normotensive individuals and 13 salt-sensitive and 14 salt-resistant blacks with essential hypertension under conditions of low (10 mEq/d) and high (250 mEq/d) salt intake. To evaluate possible racial differences in ANP secretion, we also measured plasma ANP in 6 salt-sensitive and 8 salt-resistant hypertensive whites during low and high salt intakes. Under low salt conditions, plasma ANP levels were not different in normotensive control subjects and salt-sensitive and salt-resistant hypertensive blacks. During high salt intake, plasma ANP levels did not change in control subjects and salt-resistant patients but decreased in salt-sensitive patients. ANP levels after high salt diet were lower (P < .01) in salt-sensitive than salt-resistant blacks. In hypertensive whites, high salt intake caused no significant change in plasma ANP. Under low salt conditions, plasma NO2+NO3 levels were higher (P < .05) in salt-sensitive (189 +/- 7.9 mumol/L) and salt-resistant (195 +/- 13.5 mumol/L) black patients than in control subjects (108 +/- 9.7 mumol/L). During high salt intake, plasma NO2+NO3 decreased significantly (P < .01) in both salt-sensitive (150 +/- 7.0 mumol/L) and salt-resistant (142 +/- 9.0 mumol/L) patients. These studies show that under conditions of high salt intake, salt-sensitive hypertensive blacks manifest a paradoxical decrease in ANP secretion. This abnormality may play a role in the reduced ability of these individuals to excrete a sodium load and in the sodium-induced rise in blood pressure. This study does not support the hypothesis that salt sensitivity depends on a deficit of nitric oxide production, but it suggests that high salt intake may alter the endothelium-dependent adaptation of peripheral resistance vessels.
Adult↗
Salt sensitivity is associated with insulin resistance in essential hypertension.
The relationship between salt sensitivity and insulin resistance was investigated in nondiabetic, nonobese (body mass index < or = 28) untreated patients with uncomplicated, mild-to-moderate essential hypertension. Alterations in insulin-mediated glucose disposal were assessed by means of the insulin suppression test. Subjects were classified as salt sensitive and salt resistant according to their blood pressure response to low and high salt intake. Fasting serum glucose levels were within normal limits and did not differ between salt sensitive and salt resistant hypertensives, irrespectively of the level of salt intake. Fasting serum insulin levels increased in salt sensitive patients when on a high intake of salt. The insulin suppression test revealed the existence of marked differences in insulin-mediated glucose uptake between salt sensitive and salt resistant hypertensives. Much higher steady-state glucose values (nanomoles of glucose/ liter) were obtained during the insulin suppression test in salt sensitive than in salt-resistant hypertensives (7.4+/-1.6 v 3.5+/-0.1 under low salt; and 12.5+/-1.1 v 4.3+/-0.1 under high salt intake). The product of glucose times insulin obtained at steady state during low and high salt intakes were 2.5 and 5 times greater, respectively, in salt sensitive than in salt resistant hypertensives. Therefore, the impairment in insulin-mediated glucose disposal observed in salt sensitive hypertensives was present both under low salt (60 to 70 mEq/day) and high salt intake (300 mEq/day). However, it was exacerbated under high salt intake. These results suggest that untreated salt sensitive hypertensives have a considerable impairment in insulin-mediated glucose disposal because of a state of insulin resistance. High salt intake increased BP, induced hyperinsulinemia, and worsened insulin-mediated glucose disposal only in salt sensitive patients. We propose that salt sensitivity contributes, separately from hypertension, to insulin resistance and thus be considered per se as an additional risk factor in the development of cardiovascular disease. Salt sensitivity and insulin resistance may be genetically associated conditions.
Adult↗
[Changes in calcium levels in blood and urine during various regimens of table salt intake in patients with essential arterial hypertension].
INTRODUCTION: It has been reported that changes in salt loading influence parameters of calcium metabolism in hypertensive subjects. It was also reported that response of blood pressure to salt intake is related to salt-induced increase in intracellular calcium and decrease in intracellular magnesium concentrations [1]. Several authors showed that salt-sensitive hypertensive subjects significantly decreased blood pressure after calcium intake which was emphasized by high salt intake. Resnick et al. showed that during high salt intake regimen increase in blood pressure was followed with decrease in serum calcium level, this was explained by the fact that high salt intake stimulates the calcium uptake by cells [2]. They also reported the following characteristics of hypertensive patients with additionally lower blood pressure as a response to calcium intake: salt-sensitive, low serum ionized calcium and plasma renin activity (PRA) values and high parathyroid hormonE (PTH) values and 1.25-(OH)2-D values. The aim of the study was to evaluate values of corrected and ionized serum and urine calcium in a group of salt-sensitive patients, salt-resistant patients and a whole group during normal salt-intake regimen, and a group without salt and during sodium load (10 g salt extra). MATERIAL AND METHODS: In our study, 50 untreated patients (27 women and 23 men; average age 42 +/- 9.2 yrs; average BMI 27.91 +/- 4.6 kg/m2) with essential hypertension were put on a high salt regimen (200 mmol NaCl per day) for one week after a week on a low salt diet (20 mmol NaCl per day). On the last day of the normal regimen and during the 1st, 3rd and 5th day of low salt and high salt regimens, the following follow-up was carried out: total (corrected) serum calcium level and total urine calcium level, ionized serum calcium urine creatininE level; serum albumin and daily diuresis and blood pressure. All patients had normal sodium and potassium serum concentrations. Salt intake was checked by taking a specimen of 24-hour urine considered as satisfactory if sodium excretion of 100 to 150 mmol/d (mmol per day) was noted. During the whole hospital examination, calcium intake through hospital meals was standardized to about 817 mg of calcium daily. Salt sensitivity was defined as 10 mmHg increase in mean blood pressure at the end of high vs. low salt diet. Salt sensitive group consisted of 26 patients and salt insensitive of 24 patients. RESULTS: According to sex, there was no statistically significant difference: 27 females (54%) and 24 males (46%). Average age of patients was 49 +/- 9.2 yrs, ranging from 21 to 64 with normal frequency distribution. Average body weight was 80.49 kg +/- 12.45 kg. Body height was from 150 to 192 cm with average of 170.12 +/- 10.53 cm. Average value of Body Mass Index (BMI in kg per square meter) was 27.91 +/- 4.6. In the studied patients average duration of hypertension was 6.98 +/- 6.4 yrs with non-homogeneous distribution. In 32 patients (64%) the medical history confirmed that one or more family members had hypertension. It was found that salt loading significantly decreased ionized calcium (F = 2.49; p < 0.05) and significantly increased urinary excretion of calcium (F = 5.22; p < 0.001) in salt sensitive patients in comparison with salt insensitive subjects. Serum calcium did not differ significantly during different salt intake regimens between two groups. Our study revealed no positive correlation between gender, age, BMI and family history and calcium metabolism. CONCLUSION: The findings of this study support the opinion of altered calcium metabolism in hypertensive subjects sensitive to salt intake. By demonstrated results we tried to define clinically different pathophysiologic and potentially different therapeutic subgroups in hypertensive population and to point to clinical and biochemical heterogeneity of primary hypertension.
Adult↗
Controllable gelation of methylcellulose by a salt mixture.
The effects of a salt mixture consisting of a salt-out salt (NaCl) and a salt-in salt (NaI) on the sol-gel transition of methylcellulose (MC) in aqueous solution have been studied by means of micro differential scanning calorimetry and rheometry. The salt mixture was found to have a combined effect from the salt-out and salt-in salts in the mixture, and the salt effect was dependent on the water hydration abilities of the component ions and ion concentration. At a fixed total salt concentration, the sol-gel transition temperature nicely followed a rule of mixing: Tp = m1Tp1 + m2Tp2 where Tp, Tp1, and Tp2 are the gelation peak temperatures for the MC solutions with a salt mixture, NaCl, and NaI, respectively, and mi is the molar fraction of the salt component i in the salt mixture. The linear rule of mixing proved that the effects of NaCl and NaI on the sol-gel transition of MC are completely independent. In addition, the presence of a single salt or a salt mixture in a MC solution does not change the essential mechanism of MC gelation. Therefore, the sol-gel transition of MC can be simply controlled by a salt mixture consisting of a salt-out salt and a salt-in salt. The rheological results supported the micro thermal results excellently. But the gel strength of MC containing salts was influenced by both salt type and salt concentration.
Journal Article↗
The influence of salt on the structure and energetics of supercoiled DNA.
We present a detailed computational study of the influence of salt on the configurations, energies, and dynamics of supercoiled DNA. A potential function that includes both elastic and electrostatic energy components is employed. Specifically, the electrostatic term, with salt-dependent coefficients, is modeled after Stigter's pioneering work on the effective diameter of DNA as a function of salt concentration. Because an effective charge per unit length is used, the electrostatic formulation does not require explicit modeling of phosphates and can be used to study long DNAs at any desired resolution of charge. With explicit consideration of the electrostatic energy, an elastic bending constant corresponding to the nonelectrostatic part of the bending contribution to the persistence length is used. We show, for a series of salt concentrations ranging from 0.005 to 1.0 M sodium, how configurations and energies of supercoiled DNA (1000 and 3000 base pairs) change dramatically with the simulated salt environment. At high salt, the DNA adopts highly compact and bent interwound states, with the bending energy dominating over the other components, and the electrostatic energy playing a minor role in comparison to the bending and twisting terms. At low salt, the DNA supercoils are much more open and loosely interwound, and the electrostatic components are dominant. Over the range of three decades of salt examined, the electrostatic energy changes by a factor of 10. The buckling transition between the circle and figure-8 is highly sensitive to salt concentration: this transition is delayed as salt concentration decreases, with a particularly sharp increase below 0.1 M. For example, for a bending-to-twisting force constant ratio of A/C = 1.5, the linking number difference (delta LK) corresponding to equal energies for the circle and figure-8 increases from 2.1 to 3.25 as salt decreases from 1.0 to 0.005 M. We also present in detail a family of three-lobed supercoiled DNA configurations that are predicted by elasticity theory to be stable at low delta Lk. To our knowledge, such three-dimensional structures have not been previously presented in connection with DNA supercoiling. These branched forms have a higher bending energy than the corresponding interwound configurations at the same delta Lk but, especially at low salt, this bending energy difference is relatively small in comparison with the total energy, which is dominated by the electrostatic contributions. Significantly, the electrostatic energies of the three-lobed and (straight) interwound forms are comparable at each salt environment. We show how the three-lobed configurations change slowly with ALk, resulting in branched interwound forms at higher salt. In longer chains, the branched forms are highly interwound, with bent arms. At low salt, the branched supercoils are asymmetric, with a longer interwound stem and two shorter arms. From molecular dynamics simulations we observe differences in the motions of the DNA as a function of salt. At high salt, the supercoiled chain is quite compact but fairly rigid, whereas at low salt the DNA is loosely coiled but more dynamic. Especially notable at low salt are the large-scale opening and closing of the chain as a whole and the rapid "slithering"of individual residues past one another. Toroidal forms are not detected under these conditions. However, the overall features of the open, loose supercoils found at low salt are more similar to those of toroidal than interwound configurations. Indeed,simulated x-ray scattering profiles reveal the same trends observed experimentally and are consistent with a change from closed to open forms as salt is decreased. Like the minimization studies, the dynamics reveal a critical point near 0.1 M associated with the collapse of loose to tight supercoils. Near this physiological concentration, enhanced flexibility of the DNA is noted. The collective observations suggest a potential regulatory role for salt on supercoiled DNA function, not only for closed circular DNA,but also for linear DNA with small looped regions.
Bacteriophage phi X 174↗
Effect of a chronic high-salt diet on whole-body and organ sodium contents of Dahl rats.
OBJECTIVE: To evaluate whether a high-salt diet causes retention of Na in Dahl rats. DESIGN: To compare the whole-body and organ (liver, spleen, kidney, heart, lung, femur, submaxillary gland and muscle) Na contents in Dahl salt-sensitive rats and Dahl salt-resistant rats. METHODS: Rats aged 6-10 weeks of both strains were fed a normal-salt (0.4% NaCl) or a high-salt (8% NaCl) diet. The whole-body and organs were then ashed and their respective Na contents determined. RESULTS: Salt-resistant rats fed the normal-salt diet had a higher whole-body Na content than did salt-sensitive rats. The high-salt diet increased the whole-body Na content of salt-sensitive rats significantly, but it did not increase that of salt-resistant rats. The high-salt diet caused a significant increase in the organ weight: body weight ratio for all organs of the salt-sensitive rats, except the submaxillary gland, but had no effect on the ratios for salt-resistant rats, apart from that for the kidney. The kidney, submaxillary gland and muscle Na concentrations were greater in salt-sensitive rats than they were in salt-resistant rats. Nonetheless, regardless of strain, the high-salt diet had no effect on organ and plasma Na concentrations. The high-salt diet increased the organ weights (liver, spleen, kidney, heart and lung) and the organ Na contents per kg body weight significantly for salt-sensitive rats but not for salt-resistant rats. CONCLUSIONS: A high-salt diet caused Na retention in salt-sensitive rats only and this was partially due to enlargement of the organs.
Animals↗
Neuronal nitric oxide strongly suppresses sympathetic outflow in high-salt Dahl rats.
OBJECTIVE: To investigate the effects of a selective inhibitor of neuronal nitric oxide synthase (nNOS), 7-nitroindazole, on peripheral sympathetic outflow in Dahl rats. DESIGN AND METHODS: Dahl salt-sensitive and salt-resistant rats were fed either a regular-salt (0.4% NaCl) or a high-salt (8% NaCl) diet for 4 weeks. In chronically instrumented conscious rats, renal sympathetic nerve activity (RSNA) was measured in both baroreceptor-loaded and baroreceptor-unloaded states. The baroreceptor unload was performed by decreasing arterial pressure with occlusion of the inferior vena cava. RESULTS: 7-Nitroindazole (307 micromol/kg intraperitoneally) increased resting RSNA from 24 +/- 3% to 38 +/- 6% with an increase in mean arterial pressure of 15 +/- 3 mmHg, and increased baroreceptor-unloaded RSNA from 100% to 278 +/- 16% in salt-sensitive Dahl rats receiving a high-salt diet However, 7-nitroindazole did not increase resting RSNA, but did increase baroreceptor-unloaded RSNA from 100% to 179 +/- 15%, 177 +/- 15%, and 133 +/- 4% in salt-sensitive Dahl rats receiving a regular-salt diet, salt-resistant Dahl rats receiving a high-salt diet, and salt-resistant Dahl rats receiving a regular-salt diet, respectively. The high-salt diet significantly increased the baroreceptor-unloaded RSNA more than the regular-salt diet did, in both salt-sensitive and salt-resistant rats. After administration of the vehicle for 7-nitroindazole (peanut oil), L-arginine (100 micromol/kg per min for 10 min) decreased both resting and baroreceptor-unloaded RSNA, whereas after pretreatment with 7-nitroindazole, the L-arginine-induced suppression was reversed, in Dahl salt-sensitive rats receiving a high-salt diet. CONCLUSIONS: Neuronal nitric oxide may suppress the sympathetic discharge generated before baroreflex-mediated inhibition in all rats. This neuronal nitric oxide-mediated suppression was enhanced by the salt load in both salt-resistant and salt-sensitive Dahl rats. Finally, the neuronal nitric oxide-mediated suppression in tonic peripheral sympathetic outflow may be greatly enhanced in salt-sensitive hypertension.
Animals↗
Nitric oxide and salt sensitivity.
Studies in laboratory animals suggest that altered nitric oxide (NO) production may be associated with salt sensitivity. In this investigation we determined whether the endogenous NO production was altered in salt-sensitive human subjects when salt intake was changed. Salt sensitivity was assessed from the magnitude of the blood pressure (BP) lowering obtained when the salt intake was reduced from high to a low intake. The combined urinary excretion of nitrites and nitrates, the major metabolites of NO, was employed as an index of endogenous NO production. Salt-sensitive subjects (n = 23) were older, heavier, and had greater waist-to-hip ratios and higher baseline BP than salt-resistant individuals (n = 25). In salt-sensitive subjects, mean blood pressure (MBP) decreased 11.8+/-0.7 mm Hg, and NO metabolite excretion increased from 823+/-102 to 1530+/-148 mmol/24 h, when salt intake was reduced from 316 to 28 micromol/day. NO metabolite excretion was 45% lower during high salt (0.66+/-0.1 micromol/mg creatinine) than during low salt intake (1.12+/-0.1 micromol/mg creatinine) (P < .001). In contrast, when salt intake was reduced, salt-resistant subjects exhibited no significant mean changes in BP or NO metabolite excretion. During low salt intake, NO metabolite excretion (micromol/ day) was significantly higher in salt-sensitive individuals. The magnitude of decrease of systolic blood pressure, diastolic blood pressure, or MBP induced by reducing salt intake was not related to the increase in urinary excretion of NO metabolite levels (r2 = 0.009; P = .66). In summary, to the extent that urinary NO metabolite levels reflect the activity of the endogenous NO system, our results support the view that salt sensitivity may in part be determined by an inability to increase or to sustain NO production in response to high salt. Insufficient NO production during high salt may in turn lead to altered pressure-natriuresis relationships and to an increase in BP. The possibility that the increase in BP induced by high salt intake in salt-sensitive individuals could be the key factor in reducing NO metabolite levels can not be ruled out.
Adult↗
Nitric oxide production decreases after salt loading but is not related to blood pressure changes or nitric oxide-mediated vascular responses.
BACKGROUND: Nitric oxide production is a homeostatic mechanism that may regulate blood pressure during salt loading. Salt-sensitive hypertension in animal models and in humans is characterized by increased blood pressure and decreased nitric oxide production after salt loading. It is not known if this impaired nitric oxide production is the result of hypertension or is a mechanism contributing to the blood pressure response to salt. METHODS AND RESULTS: The effects of salt loading on blood pressure, nitric oxide-mediated vasodilation and nitric oxide production were measured in 25 normotensive subjects after 6 days on either a high (400 mmol/day) or low (10 mmol/day) sodium, low nitrate diet. Mean arterial pressure increased during the high-salt diet [4 +/- 1 mmHg (mean +/- SEM)] in 12 subjects and remained unchanged or decreased (-4 +/- 1 mmHg) in 13 subjects. Plasma nitrite and nitrate, a measure of nitric oxide production, decreased significantly from 39 +/- 3.3 micromol/l during the low-salt diet to 22.4 +/- 2.4 micromol/l during the high-salt diet (P = 0.0001). However, changes in mean arterial pressure from low- to high-salt diet did not correlate with changes in plasma nitrite and nitrate (r = 0.14, P = 0.51). Forearm blood flow increased significantly (P <0.0001) in response to mental stress, a nitric oxide-mediated response, but was not affected by sodium intake (from 7.8 +/- 0.9 to 11.2 +/- 1.4 ml/min per 100 ml during low salt versus 8.5 +/- 1.2 to 10.4 +/- 1.3 ml/min per 100 ml during high salt,P = 0.3). CONCLUSIONS: Salt loading results in a decrease in nitric oxide production in both salt-sensitive and salt-resistant normotensive subjects, which is independent of changes in blood pressure and does not affect the nitric oxide-mediated vascular response to mental stress. In contrast to salt-resistant animal models, salt loading in healthy subjects does not increase nitric oxide production. Therefore, the increased blood pressure response to salt loading may occur through mechanisms other than nitric oxide, or salt-sensitive individuals are more sensitive to the reduced nitric oxide production that occurs after salt loading in both salt-sensitive and salt-resistant subjects.
Adult↗
Alpha 2-adrenoceptors in brain and kidney during development of hypertension in Dahl-Iwai salt-sensitive rats.
BACKGROUND: Both renal and extrarenal factors have been considered to contribute to the development of hypertension in Dahl salt-sensitive rats, but contents of both factors have not been established precisely. AIM: To clarify the role of those factors in the sympathetic nervous system, we examined the regulation of alpha2-adrenoceptors in the lower brainstem and the renal tubular basolateral membranes simultaneously during the development of salt-induced hypertension in Dahl-Iwai salt-sensitive rats. METHODS: Dahl-Iwai salt-sensitive or resistant rats were fed a high (8.0% NaCl)- or low (0.3%)- salt diet from 4 to 6 or 10 weeks of age. At 4, 6 and 10 weeks of age, the plasma membranes of the lower brainstem and the renal tubular basolateral membranes were obtained simultaneously and alpha 2-adrenoceptors were quantified by a radioligand binding assay using 3H-rauwolscine. RESULTS: In the salt-sensitive rats, systolic blood pressure was significantly higher in those fed a high-salt diet than in those fed a low-salt diet. In the salt-resistant rats, both the high- and the low-salt groups showed similar blood pressure levels. At 6 weeks of age, alpha 2-receptor densities of the salt-sensitive rats fed a high-salt diet were lower in the lower brainstem and higher in the renal basolateral membranes than those fed a low-salt diet. In contrast, in the salt-resistant rats, both the high- and the low-salt groups had similar densities. At 10 weeks of age, the difference between the high- and the low-salt groups in the salt-sensitive rats disappeared in both the brainstem and the renal basolateral membranes. CONCLUSIONS: Alpha 2-adrenoceptor regulation in the brainstem and the renal basolateral membranes differs between Dahl-Iwai salt-sensitive and salt-resistant rats. The modulation of alpha 2-adrenoceptors by a high salt intake may be essential particularly in the early phase of the development of salt-induced hypertension.
Animals↗
Does the Sabra hypertension-prone rat represent a model of salt or mineralocorticoid sensitivity?
OBJECTIVES: Since the Sabra experimental model of hypertension was developed, it has been known as a model of salt-susceptible hypertension. Because the hypertensive response of the Sabra hypertension-prone strain (SBH/y) is classically elicited by salt loading with a combination of deoxycorticosterone acetate (DOCA) and salt, doubt has now been cast on whether the hypertensive response is due to sensitivity to salt or to mineralocorticoids. The present study was designed to resolve this question. MATERIALS AND METHODS: We studied the blood pressure response of SBH/y to various modes of salt loading. Animals were salt-loaded by administration of: 1% NaCl in drinking water and subcutaneous implantation of a 25 mg DOCA pellet (DOCA-salt); DOCA alone; 1% NaCl in drinking water alone; or 8% NaCl in chow alone. Blood pressure was determined by the tail-cuff method in awake and undisturbed animals. RESULTS: Within 4 weeks, the DOCA-salt treatment elicited the full hypertensive response previously reported in the SBH/y strain. Salt loading with 8% NaCl in chow reproduced the full hypertensive response observed with DOCA-salt, except that it occurred only after 7 weeks of treatment. Salt loading with DOCA alone raised blood pressure moderately and to a maximal level within 3 weeks; the magnitude of the blood pressure response was, however, significantly smaller than that observed with DOCA-salt or 8% NaCl in chow. Administration of 1% NaCl in water alone elicited no hypertensive response. CONCLUSIONS: The hypertensive response to salt loading in the Sabra experimental model of hypertension is an expression primarily of salt sensitivity, as it can be fully reproduced with salt alone, but not with DOCA alone. The use of the DOCA-salt mode of salt loading in this model, as opposed to salt loading with 8% salt in chow, is a useful way of accelerating the development of salt-sensitive hypertension in SBH/y, which shortens, and therefore facilitates, phenotyping.
Animals↗
Mechanisms by which low salt condition increases sensitivity of thyroid stimulating antibody assay.
Mechanisms for high sensitivity in the assay of thyroid stimulating antibody under low salt (NaCl-deprived) hypotonic condition were analyzed using FRTL-5 rat thyroid cells. First, intracellular and extracellular cAMP contents after stimulations with TSH and Graves' immunoglobulin (Ig) were measured under both low salt (hypotonic) and high salt (isotonic) conditions. Higher total and much higher extracellular cAMP production were observed under the low salt condition. Under the high salt condition, the intracellular cAMP content reached a plateau after 10 min, whereas it increased progressively up to 120 min under the low salt condition. Thus, other cellular mechanisms, as well as increase in membrane permeability, seem to be involved in the enhanced response under the low salt condition. On the other hand, pretreatment of the cells with low salt solution without stimulator resulted in a decrease in subsequent cAMP response to TSH or Graves' Ig. Furthermore, [125I]bovine TSH binding to the cells under low salt condition also decreased after the cells were pretreated with the low salt solution. Scatchard analysis revealed that this decrease was due to a decrease in the Cmax of the low affinity binding site of the TSH receptor. Presence of stimulatory ligands to the TSH receptor from the beginning of exposure of the cells to low salt conditions was considered necessary. When the cells had been pretreated at 4 C with stimulator preparations in low salt condition, subsequent incubation at 37 C without stimulator resulted in more cAMP production than the case of high salt pretreatment. Moreover, low salt ligand-free incubation after the high salt binding resulted in higher cAMP production than high salt ligand-free incubation after the low salt binding. Thus, both initial binding and incubation under the low salt condition appear capable of augmenting cAMP production. The fact that the sensitivity of the low salt assay to Graves' Ig was higher than that to bovine TSH was found to relate closely to the increase in initial binding. In conclusion, augmentation of cAMP production under low salt conditions is considered to be related not only to increased ligand binding and increased membrane permeability, but also to some alterations of postreceptor mechanisms during incubation. The proposed postreceptor mechanisms seem to be induced by stimulator binding, which prevents the TSH receptor from damage and promotes intracellular cAMP production progressively. Details of this remain to be elucidated.
Animals↗
The effects of high dietary calcium on salt-induced hypertension in rats.
The effects of dietary salt-loading and concurrent administration of dietary calcium on water and electrolyte excretion in Sprague-Dawley rats have been studied. The total salt consumed by salt-loaded rats was significantly higher than that of control rats (P < 0.05). The total salt consumed by salt-loaded calcium fed rats was also higher (P < 0.05) than that of control rats but it was slightly lower (P < 0.05) than the consumption by the salt-loaded. Rats fed only high calcium diet had the least salt consumption. The total water intake was also highest (P < 0.05) in the salt-loaded rats when compared with either control rats, salt-loaded-calcium-fed rats or calcium-fed rats. Urinary water excretion was highest (P < 0.05) in salt-loaded-calcium-fed rats followed by salt-loaded rats and calcium-fed rats while the control rats had the least. Similarly, the sodium excretion was highest in salt-loaded-calcium-fed rats followed by salt-loaded rats and calcium-fed rats and control rats respectively. Potassium excretion was highest in salt-loaded-calcium-fed rats followed by salt-loaded rats and calcium-fed rats while the control rats had the least excretion of potassium. Serum sodium concentrations were identical in all the groups although in salt-loaded rats and salt-loaded-calcium-fed rats the values were slightly higher than those of controls. However, serum potassium concentration was lowest in salt-loaded rats and calcium-fed rats while the values for salt-loaded-calcium-fed rats was not significantly different from that of control. The results of this study suggest that increase in dietary calcium intake reduces the increase in blood pressure resulting from salt-loading and this is accompanied by an increase in water and sodium excretion.
Animals↗
Clustering of cardiovascular risk factors in salt-sensitive patients with essential hypertension: role of insulin.
Hyperinsulinemia, insulin resistance, or both have been described in a proportion of patients with essential hypertension, and also are considered a risk for atherosclerotic cardiovascular disease. In this study, we have examined whether salt sensitivity and hyperinsulinemia are associated in patients with essential hypertension. We have measured blood insulin and glucose response to an acute oral glucose load in a group of hypertensive patients, classified according to their salt sensitivity. To determine salt sensitivity, patients received a diet containing a low (20 mEq/day) Na+ intake for 1 week followed by a high (250 mEq/day) Na+ intake for 1 week more. Twenty-nine patients were classified as salt sensitive, and 23 as salt resistant. Baseline plasma glucose and insulin were not different between salt-sensitive and salt-resistant patients. Following an oral glucose load, the area-under-the curve of glucose was greater (P < .05) in salt-sensitive than in salt-resistant hypertensive patients (900 +/- 26.4 and 810 +/- 29.1 mmol/L x 2 h, respectively). The area-under-the curve of insulin was greater (P < .01) in salt-sensitive (52,664 +/- 3,666 pmol/L x 2 h) than in salt-resistant patients (37,977 +/- 3,300 pmol/L x 2 h). A direct correlation was present between insulin area-under-the curve and salt sensitivity (r = 0.26), but did not reach statistical significance (P < .06). Salt-sensitive patients manifested increased serum levels of total cholesterol, LDL-cholesterol and increased urinary albumin excretion when compared with salt-resistant patients. In conclusion, these studies have demonstrated that in response to an oral glucose load, salt-sensitive patients with essential hypertension manifest increased insulin secretion. The studies have confirmed the presence of increased urinary albumin excretion and serum levels of atherogenic lipoproteins in salt-sensitive compared with salt-resistant patients. In salt-sensitive hypertensive patients, hyperinsulinemia, hyperlipidemia and microalbuminuria form a cluster with possible atherogenic potential. Salt sensitivity can be a marker for increased cardiovascular risk in patients with essential hypertension.
Adult↗
Determinants of salt use in cooked meals in The Netherlands: attitudes and practices of food preparers.
OBJECTIVE: To assess current habits of using salt and other seasonings in food preparation, and to investigate the psychosocial determinants of salt use. In addition we examined differences in salt consumption and psychosocial determinants with respect to stages of change and socio-economic classes. SUBJECTS AND METHODS: 400 adults were interviewed to determine: 1) use of salt and other seasonings in food preparation; 2) added table salt; 3) consumption of foods with high salt content; and 4) psychosocial determinants of salt consumption. Subjects were divided into 5 stages of change for salt content of the cooked meal: precontemplation, contemplation, decision, action and maintenance. RESULTS: Salt appeared to be the type of seasoning mostly added in food preparation. Frequently used seasonings containing no added salt were pepper, onion, nutmeg, garlic, curry, sweet pepper powder, parsley, and bay-leaf. Spearman correlation coefficients between added cooking salt and taste attitude, health attitude, social influence and self-efficacy were 0.51, 0.14, 0.36, and 0.32 respectively. Correlations between consumption of foods with high salt content and convenience attitude, taste attitude, health attitude and self-efficacy were 0.41, 0.27, 0.18 and 0.21 respectively. Subjects in maintenance of low salt consumption, used less salt than subjects in precontemplation. Socio-economic status only showed an effect on the use of foods with high salt content. CONCLUSION AND PRACTICAL IMPLICATIONS: Health aspects did not play a major role in salt intake, whereas taste attitude was an important predictor of added cooking salt. Attempts to reduce cooking salt should be directed at satisfying taste. Nutrition education tailored to stages of change may be very helpful in decreasing salt consumption.
Adult↗
Blunted parasympathetic modulation in salt-sensitive patients with essential hypertension: evaluation by power-spectral analysis of heart-rate variability.
OBJECTIVE: To evaluate autonomic nervous function by power-spectral analysis of heart-rate variability in salt-sensitive and non-salt-sensitive patients with essential hypertension under the conditions of low and high salt intakes. DESIGN AND METHODS: The blood pressures, heart rates, and electrocardiogram R-R intervals of 20 hypertensive patients were measured at intervals of 30 min during a 24 h period using a portable recorder (TM-2425) on the last day of the high- (250 mmol NaCl/day) and low-salt (25 mmol NaCl/day) diet periods. The patients whose 24 h average mean blood pressures were increased by more than 10% by the high salt intake were defined as salt-sensitive (n = 10); the other patients were considered non-salt-sensitive (n = 10). Power-spectral analysis of R-R intervals was performed to obtain the low-frequency component (0.05-0.15 Hz) and the high-frequency component (0.15-0.40 Hz). RESULTS: The average 24 h blood pressure in the salt-sensitive patients was increased by the high salt intake [by 19.1 +/- 2.0/9.1 +/- 0.8 mmHg (mean +/- SEM)], whereas the heart rate did not change. In contrast, the increase in 24 h blood pressure in the non-salt-sensitive patients caused by the high salt intake was not significant and the heart rate was decreased significantly by the high salt intake (by 5.9 +/- 1.4 beats/min). The high-salt diet increased significantly the high-frequency component and decreased the low-frequency:high-frequency component ratio both during the daytime and during the night-time for the non-salt-sensitive patients. In contrast, the high-frequency component and the night-time low-frequency: high-frequency component ratio of the salt-sensitive patients did not respond to dietary salt manoeuvres. CONCLUSIONS: Responses of the parasympathetic and sympathetic nervous systems to dietary salt manoeuvres were blunted in salt-sensitive patients. These altered modulations of the autonomic nervous system may contribute to the salt sensitivity of the blood pressure in patients with essential hypertension.
Blood Pressure↗