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PubMed2006

Renal NF-kappaB activation and TNF-alpha upregulation correlate with salt-sensitive hypertension in Dahl salt-sensitive rats.

Molecular mechanisms of salt-sensitive (SS) hypertension related to renal inflammation have not been defined. We seek to determine whether a high-salt (HS) diet induces renal activation of NF-kappaB and upregulation of TNF-alpha related to the development of hypertension in Dahl SS rats. Six 8-wk-old male Dahl SS rats received a HS diet (4%), and six Dahl SS rats received a low-sodium diet (LS, 0.3%) for 5 wk. In the end, mean arterial pressure was determined in conscious rats by continuous monitoring through a catheter placed in the carotid artery. Mean arterial pressure was significantly higher in the HS than the LS group (177.9 +/- 3.7 vs. 109.4 +/- 2.9 mmHg, P < 0.001). There was a significant increase in urinary albumin secretion in the HS group compared with the LS group (22.3 +/- 2.6 vs. 6.1 +/- 0.7 mg/day; P < 0.001). Electrophoretic mobility shift assay demonstrated that the binding activity of NF-kappaB p65 proteins in the kidneys of Dahl SS rats was significantly increased by 53% in the HS group compared with the LS group (P = 0.007). ELISA indicated that renal protein levels of TNF-alpha, but not IL-6, interferon-gamma, and CCL28, were significantly higher in the HS than the LS group (2.3 +/- 0.8 vs. 0.7 +/- 0.2 pg/mg; P = 0.036). We demonstrated that plasma levels of TNF-alpha were significantly increased by fivefold in Dahl SS rats on a HS diet compared with a LS diet. Also, we found that increased physiologically relevant sodium concentration (10 mmol/l) directly stimulated NF-kappaB activation in cultured human renal proximal tubular epithelial cells. These findings support the hypothesis that activation of NF-kappaB and upregulation of TNF-alpha are the important renal mechanisms linking proinflammatory response to SS hypertension.

Animals↗
PubMed2002

Abnormal regulation of ENaC: syndromes of salt retention and salt wasting by the collecting duct.

Although the aldosterone-responsive segments of the nephron together reabsorb <10% of the filtered Na+, certain single-gene defects that affect the epithelial Na+ channel (ENaC) in the luminal membrane of the collecting duct (CD) or its regulation by aldosterone cause severe hypertension, whereas others cause salt wasting and hypotension. These rare defects illustrate the key role of the distal nephron in maintaining normal extracellular volume and blood pressure. Genetic defects that increase the Cl- conductance of the junctional complexes may also lead to salt retention and hypertension. Less dramatic alterations in regulatory actions of other hormones such as vasopressin (VP), either alone or with other genetic variations, diet, or environmental factors, may also produce Na+ retention or loss. Although VP acts primarily to regulate water balance, it is also an antinatriuretic hormone. Elevated basal plasma VP levels, and/or augmented VP release with increased Na+ intake, have been linked to essential hypertension in humans and in animal models of congestive heart failure and cirrhosis. Norepinephrine, dopamine, and prostaglandin E2 can inhibit the antinatriuretic effects of VP, and changes in the actions of these autocrine and paracrine regulators may also be involved in abnormal regulation of Na+ reabsorption.

Animals↗
PubMed1988

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

To determine if alterations of electrolyte balance or sympathetic nervous system activity are present in Dahl salt-sensitive rats (DS) before the onset of hypertension, we compared electrolyte balances, extracellular fluid volume (inulin space), plasma volume (radiolabeled albumin), and norepinephrine turnover in peripheral tissues (heart and interscapular brown fat) in prehypertensive DS and Dahl salt-resistant rats (DR). Animals were maintained for 5 to 7 days on either a "normal" or high NaCl diet. Tissue norepinephrine turnover was evaluated by measuring the rate at which norepinephrine content decreased following tyrosine hydroxylase inhibition with alpha-methyl-p-tyrosine. Blood pressure was higher (p less than 0.05) in DS (135 +/- 2 [SE] mm Hg) than in DR (129 +/- 2 mm Hg) and was not affected by the diets. Extracellular fluid volume and net Na+ and Cl- balances did not differ between DS and DR. However, plasma volume was greater in DS than in DR (p less than 0.05). In both fat and heart, norepinephrine turnover was decreased by dietary NaCl loading in DR (p less than 0.01), but not in DS. Thus, the tendency of the DS to become hypertensive with high NaCl intake may be related to the combined effects of an increased plasma volume and the failure of high dietary NaCl to inhibit peripheral sympathetic nervous system activity.

Animals↗
PubMedDate not supplied

Aortic responses to vanadate: independence from (Na,K)-ATPase and comparison of Dahl salt-sensitive and salt-resistant rats.

Vanadate at doses from 10(-4.5) to 10(-3) M caused a dose-dependent contraction of the rat aorta in vitro. Aortas of Dahl salt-hypertension sensitive (S) rats responded to vanadate with a greater contraction than Dahl salt-hypertension resistant (R) rats. In contrast, S and R aortic responses to depolarization with potassium were equal, and responses to norepinephrine were less in S than R. The mechanism by which vanadate causes the aortic response was studied in S rats. In aortic smooth muscle sodium-loaded by exposure to low potassium media followed by a norepinephrine-induced contraction, a relaxation induced with 5 mM potassium was not influenced by 10(-3) M vanadate. Since this potassium-induced relaxation is known to be a reflection of (NaK)-ATPase activity, these data show that vanadate (up to 10(-3) M does not inhibit (Na,K)-ATPase in intact smooth muscle cells although it is a known potent inhibitor of (Na,K)-ATPase in isolated cell membrane preparations. Response to vanadate was not changed by alpha-blockade with phentolamine or by blocking (Na,K)-ATPase with ouabain. Vanadate contraction was blocked by 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene, a known inhibitor of anion transport, suggesting that vanadate anions must enter smooth muscle cells to induce contraction.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

In vivo production of prostaglandin I2 in Dahl salt-sensitive and salt-resistant rats.

Prostaglandin I2 (PGI2, prostacyclin), a potent vasodilator synthesized by the blood vessels, has been postulated to play a role in hypertension. The purpose of our study was to test this hypothesis by monitoring the in vivo production of PGI2 in Dahl salt-sensitive (S) and salt-resistant (R) rats under normal and high sodium intake. The 24-hour urinary excretion of two endogenous metabolites of PGI2, 2-,3-dinor-6-oxo-PGF1 alpha, an 2,3-dinor-13,14-dihydro-6,15-dioxo-PGF1 alpha was measured by combined gas chromatography-mass spectrometry (GC-MS) and used as an index of the total production of PGI2 by the animals. The pattern of urinary excretion of these two metabolites in the R and the S rats during the control period indicated that, under normal conditions, early in life the basal production of PGI2 was the same in both groups of rats. Following the chronic administration of a high sodium diet (8.1% sodium chloride, starting at 36 days of age), a significant and sustained increase in the urinary excretion of 2,3-dinor-6-oxo-PGF1 alpha was documented in the R rats (from 37 +/- 7 ng/24 hrs at age 35 days to 63 +/- 7, 52 +/- 4, and 56 +/- 10 ng/24 hrs at 50, 60, and 80 days, respectively), whereas the urinary levels of this metabolite decreased slightly in the S rats (from 41 +/- 7 ng/24 hrs at age 35 days to 25 +/- 5, 30 +/- 6, and 28 +/- 9 ng/24 hrs at 50, 60, and 80 days, respectively). During the same period, the R rats remained normotensive (103 +/- 5 mm Hg, systolic pressure) while the arterial pressure of the S rats increased gradually (to 142 +/- 8 and 180 +/- 19 mm Hg at ages 60 and 80 days, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Differential effect of salt loading on sodium and lithium excretion in Dahl salt-resistant and -sensitive rats.

Fractional excretion of lithium, as a marker for proximal sodium reabsorption, was determined in normotensive Dahl S rats (susceptible to NaCl hypertension) and Dahl R rats (resistant to NaCl hypertension) before and following an acute sodium load. Baseline mean arterial pressures, inulin clearances, sodium excretion rates, and fractional lithium clearances were not different between the R and S rats. Following the salt loading and despite similar mean arterial pressures and degree of volume expansion, the glomerular filtration rate, urinary flow rates, and absolute sodium excretion rates were greater in R than S rats. The fractional excretion of lithium was also greater in R than S rats. These data demonstrate that, at equal mean arterial pressures, Dahl S rats have a reduced capacity for sodium excretion, and that this defect is present prior to the development of hypertension. Furthermore, the observation that these animals also have a lower fractional lithium excretion during volume expansion suggests that salt loading reduces proximal tubule reabsorption to a lesser extent in Dahl S than R rats. These data suggest that the subnormal sodium and water excretion observed after sodium loading in S rats may be partially due to an abnormality in proximal tubule sodium handling.

Animals↗
PubMed1987

Partial characterization of atrial natriuretic factor in the hearts of Dahl salt-sensitive and salt-resistant rats.

Atria of adult Dahl salt-sensitive rats contain more atrial natriuretic factor (ANF) than those of Dahl salt-resistant rats, as measured by RIA. This strain difference was not seen at 15 days of age, but was observed at and after 30 days of age. Neither a sodium-deficient diet nor an 8% NaCl diet started as early as 2 weeks of age altered this strain difference, although high dietary NaCl was associated with reduced atrial ANF concentration. In addition, no qualitative differences were found in the S and R ANF precursor, as assessed by 1) in vitro translation of atrial mRNA followed by immunoprecipitation of the ANF precursor and polyacrylamide gel electrophoresis, and 2) fractionation of S and R atrial extracts by reverse phase HPLC. These findings support the view that the S vs. R strain difference in atrial ANF concentration is more likely to arise from genetic control of regulatory phenomena than from alterations in the structural part of the ANF gene.

Age Factors↗
PubMed1987

Quantification of messenger ribonucleic acid for atrial natriuretic factor in atria and ventricles of Dahl salt-sensitive and salt-resistant rats.

The levels of atrial natriuretic factor (ANF) and the mRNA for ANF were measured in the left ventricles of Dahl salt-sensitive (S) and salt-resistant (R) rats. ANF and ANF mRNA were both much higher in ventricular tissue of newborn rats of both strains compared to young adults, which represents the normal developmental pattern. There was no strain difference between S and R when the rats were young (1.5 months of age), but in older animals (8.5 months of age), when S rats were markedly hypertensive, there was a 5- to 10-fold increase in both left ventricular ANF and left ventricular ANF mRNA in S, but not R, rats. Atrial ANF mRNA was not similarly increased in hypertensive S rats. The ANF levels present in ventricles could not be accounted for by contamination with plasma ANF. Moreover, HPLC analysis of the forms of ANF in ventricles of newborn and hypertensive S rats showed that immunoreactive ANF in ventricles was present mainly in the same precursor form found in atria and not the shorter peptide form found in plasma. Northern blot analysis showed that ANF mRNA for atria and ventricles were the same size. It is concluded that in the S rat the heart left ventricle responds to hypertension by increasing production and storage of ANF.

Aging↗
PubMed1989

Structural differences in the renin gene of Dahl salt-sensitive and salt-resistant rats.

Genomic libraries in lambda EMBL4 phage were constructed from both inbred Dahl salt-hypertension-sensitive (S) and inbred Dahl salt-hypertension-resistant (R) rats. Overlapping clones containing the renin genes were isolated from these libraries by screening with a renin cDNA probe. Clones were characterized by a combination of restriction mapping and Southern blot analysis. The results showed that the S-rat renin gene is remarkably different from the R-rat renin gene. The major differences are 1) a 1.2-kilobase (kb) insertion in the first intron of the S-gene which accounts for most of the restriction fragment length polymorphisms found in the renin genes between S and R strains, such as those generated with Bg/II [2.7 kb (S)/1.5 kb (R)], EcoRI [6.4 kb (S)/5.2 kb (R)], and HindIII [9.6 kb (S)/8.4 kb (R)]; 2) an additional HindIII site located at the 3' end of the R-gene which accounts for another HindIII restriction fragment length polymorphisms [25 kb (S)/22 kb, 3.4 kb (R)]; 3) two SmaI sites at the 5' flanking region of the first exon of the S-gene, whereas there is only one SmaI site in the corresponding region of the R-gene; and 4) three AvaI sites in the first intron of the S-gene in contrast to two AvaI sites in the same region of the R-gene These differences in the renin genes of Dahl rats might affect renin gene expression, which could account for the known strain differences in plasma and tissue renin activities. These structural studies provide a basis for genetic investigation into the relationship of the renin gene to blood pressure in Dahl rats.

Animals↗
PubMed1978

Plasma mineralocorticoids, plasma renin, and urinary kallikrein in salt-sensitive and salt-resistant rats.

Plasma aldosterone, deoxycorticosterone (DOC), 18-hydroxy-deoxycorticosterone (18OH-DOC), and corticosterone were measured in Dahl salt-sensitive (S) and salt-resistant (R) rats. Plasma corticosterone and DOC were not different between strains but plasma aldosterone was decreased and plasma 18OH-DOC increased in S compared to R. Plasma renin activity and urinary kallikrein excretion were both lower in S than R. Urinary kallikrein is known to vary directly with mineralocorticoid activity and 18OH-DOC is a weak mineralocorticoid. The lower urinary kallikrein in the presence of elevated 18OH-DOC could mean that urinary kallikrein differences between S and R are under independent genetic control from 18OH-DOC.

18-Hydroxydesoxycorticosterone↗
PubMed1981

Effects of dexamethasone on excretion of urinary kallikrein and urinary protein in Dahl salt-sensitive and salt-resistant rats.

The effect of glucocorticoid treatment on urinary kallikrein excretion was assessed in Dahl salt-hypertension susceptible (S) and salt-hypertension resistant (R) rats. A single dose of dexamethasone (100 micrograms) caused a marked water diuresis and a slight decrease in urinary kallikrein excretion in both S and R rats. A single dose of dexamethasone also caused the S rat to excrete massive amounts of protein into the urine, almost 3-fold higher than S rats treated with oil; the effect on R rat urinary protein was similar, but less severe. Daily administration of dexamethasone (100 micrograms/day) for 7 days caused marked suppression of urinary kallikrein excretion in both S and R rats. Increased urinary protein following chronic treatment was still evident in the dexamethasone-treated S rats but not in the dexamethasone-treated R rats. Chronic glucocorticoid treatment probably inhibits urinary kallikrein activity by suppressing pituitary and adrenal function which would remove the stimulatory effect of aldosterone on urinary kallikrein excretion. There was no evidence for a stimulatory role of glucocorticoids on urinary kallikrein.

Animals↗
PubMed1987

Dietary sodium intake and urinary dopamine and sodium excretion during the course of blood pressure development in Dahl salt-sensitive and salt-resistant rats.

Recent studies have suggested that dopamine (DA) formed within the kidney may play an important role in promoting sodium excretion, and that renal production and excretion of DA is determined by dietary sodium intake. Inasmuch as increased sodium consumption produces hypertension in Dahl salt-sensitive (DS) rats but not in Dahl salt-resistant (DR) rats, the present study was designed to examine the relationship between sodium consumption and urinary excretion of DA in these rats. DS and DR rats were placed on either high sodium chloride (8%) or low sodium chloride (0.4%) diets at 4 weeks of age and their systolic blood pressure (SBP), urine volume, urinary sodium and catecholamine excretion were measured once every week for the next 4 weeks. High sodium chloride diet increased SBP in DS rats at 6 weeks of age and SBP continued to rise until they were 8 weeks old. The SBP of DR rats did not reach hypertensive levels when they were given high sodium chloride diet. The SBP of DS rats on low sodium chloride diet was significantly higher than DR rats on the same diet. The urinary DA excretion increased with age in all four groups of rats and was similar when they were 8 weeks old. However, both DS and DR rats on high sodium chloride diet excreted greater amounts of sodium and had increased urine volume compared to the DS and DR rats on low sodium chloride diet. There were no significant differences in urinary NE or E excretion in these four groups of rats. Kidney levels of DA and NE were significantly lower in DS compared to DR rats on high sodium chloride diet. These results show that although there are no differences in urinary DA excretion between rats on low and high sodium intake, both DS and DR rats on high sodium chloride diet are able to exhibit a natriuretic response. The DS rats eliminate sodium at the expense of an elevated SBP whereas DR rats stay normotensive. Therefore, it appears that alterations in mechanisms controlling renal vascular resistance rather than sodium excretion are responsible for the development of hypertension in DS rats.

Animals↗
PubMed1984

Effects of dietary salt, fat, and carbohydrate on fluid and salt consumption of rats.

Studies were conducted to investigate the influence of dietary sodium chloride (NaCl), fat, and carbohydrate on NaCl preferences of rats. Both long-term (48 hr) and short-term (20 min) two-bottle preference tests were used. Rats were fed either a basal salt (1.17%) diet or high salt (8.37 to 8.59%) diets in which the level of sucrose was modified by substitution with either corn oil or cornstarch. Water and NaCl consumption was measured in 48-hr two-bottle preference tests using various concentrations (0.005 to 0.5 M) of NaCl paired with water. The results of these studies suggest that changes in fluid consumption were accounted for by an increase in water consumption which was inversely related to the sucrose to starch ratio and directly related to the NaCl content of the diets. A reduction in NaCl consumption was observed only during the short-term (20 min) tests.

Animals↗
PubMed2001

Hemodynamic effects of agmatine in Dahl salt-sensitive hypertensive and Dahl salt-resistant rats.

The hemodynamic effects of agmatine were investigated in anaesthetized Dahl salt-sensitive (DS) hypertensive and Dahl salt-resistant (DR) rats. The results are as follows. (1) Agmatine (1, 10, 20 mg/kg i.v.) decreased heart rate (HR), mean arterial pressure (MAP), left ventricular blood pressure (LVP), the first derivative of LVP (LV dp/dt), cardiac index (CI) and total peripheral resistance index (TPRI) in a dose-dependent manner in both DS and DR rats, and the decreases in MAP, LVP, +/- LV dp/dtmax and TPRI at the same dose of agmatine in DR rats were less than those in DS hypertensive rats. Specifically, agmatine at high dose (20 mg/kg) induced a delayed increment of hemodynamic parameters in DS hypertensive rats, but not in DR rats. (2) Idazoxan (2.5 mg/kg), an antagonist for I2 over I1-imidazoline receptors and alpha 2-adrenoceptor receptors (alpha 2-AR), only partially blocked the effects of agmatine (10 mg/kg). (3) Yohimbine (4 mg/kg), a selective alpha 2-AR antagonist, also partially attenuated the effects of agmatine. (4) Efaroxan (2.5 mg/kg), a selective antagonist for I1 over I2-imidazoline receptors and alpha 2-AR, could completely block the effects of agmatine. Taken together, the results indicate that agmatine can dose-dependently decrease HR, MAP, LVP, +/- LV dp/dtmax, CI and TPRI in DS hypertensive and DR normotensive rats. The hemodynamic effects of agmatine are mediated mainly by I1-IR with the participation of I2-IR and alpha 2-AR.

Agmatine↗
PubMed2003

[Isolation and characterization of SIR73 gene fragment in salt resistant mutant of wheat involved in salt stress].

cDNA-AFLP (amplified fragment length polymorphism) is used to isolate genes differentially expressed in two wheat lines with the different resistance to NaCl derived from a single seed. A lot of cDNA fragments related to salt tolerance are obtained. Of with the number 73 cDNA fragment encodes for a transcription factors with an 32% similarity to human transcription factors in the relative amino acid which is named SIR73. Northern analysis confirms that SIR73 is strongly induced by NaCl stress and the expression in SR is more strongly induced than in SS.SIR73 may be involved in the regulation of gene expression in salt stress in wheat.

English Abstract↗
PubMed1991

Effect of the adrenal inhibitor trilostane on the morphology of the adrenocortical cells of Dahl salt-sensitive and Dahl salt-resistant rats.

The effects of trilostane on the adrenal cortex of Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rats were investigated morphometrically, histochemically, ultrastructurally and biochemically. The statistical analysis indicated that trilostane induced a significant increase in the adrenal weight and the surface area of cells and nuclei in the zona fasciculata (ZF) of the adrenal cortex of DS and DR rats (P less than O.OI). DS rats treated with trilostane revealed marked accumulation of large amounts of lipid droplets and a decrease in the activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) in the ZF. Ultrastructurally, the mitochondria of the ZF in DS rats treated with trilostane revealed swelling of matrix with a loss of cristae and occasional interruption of the membranes of mitochondria. Some of them had a continuity with lipid vacuoles or SER, presenting a characteristic 'feather'-like appearance. Other characteristic findings in DS rats treated with trilostane were a marked villous proliferation of plasma membranes with numerous dense bodies, occasional coated pits, and pinocytic vesicles in the outer portion of the ZF. In DS and DR rats the plasma level of ACTH increased, and corticosterone decreased significantly (P less than O.OI) after treatment with trilostane. These morphological alterations were considered to be an expression of the inhibitory effects of trilostane on the adrenal steroidogenesis in DS and DR rats, more especially in DS rats. Simultaneously there were confirmed morphological alterations in the cells of the ZF, reflecting the feedback stimulation of endogenous ACTH. The cells of the ZF of DS rats were more responsive to suppression by trilostane than those of DR rats.

3-Hydroxysteroid Dehydrogenases↗
PubMed1990

[Binding sites of imidazolines. Study with (3H)-idazoxan in renal cortex of Sabra salt-sensitive (SBH) and salt-resistant (SBN) rats].

Imidazoline binding sites have been characterized in organs modulating blood pressure, such as brain and kidney with (3H)-p-aminoclonidine and (3H)-Idazoxan respectively. However, the pharmacological characteristics of the imidazoline-preferring binding sites differ considerably depending on the species investigated and the radioligand used. Little is known about the physiological relevance of the non-adrenergic (3H)-idazoxan binding sites. As some imidazolines and certain alpha-adrenoceptor agonists possess antihypertensive activity, an alteration of these binding sites should be considered as a possible causes in the development of hypertension. In the present study, we performed binding studies with the imidazoline ligand (3H)-idazoxan in renal cortex of hypertensive salt-sensitive (SBH) and normotensive salt-resistant (SBN) Sabra rats. (3H)-idazoxan binding capacities were higher in SBH than in SBN rats. Competition studies have shown for (3H)-idazoxan specific binding non-adrenergic characteristics exclusively. In these both substrains, (3H)-idazoxan binding exhibit pharmacological profile of imidazoline binding sites. However, theses sites have also high affinity for guanidino compounds and amiloride. Surprisingly, amiloride and some analogues were significantly more potent in SBN than in SBH rats. From this study, it is difficult to elucidate the physiological role of imidazoline binding sites in renal cortex. However, differences observed between SBN and SBH suggest that these sites may play a role in the development of hypertension in Sabra rats.

Adrenergic alpha-Antagonists↗
PubMed1988

Na+/K+-ATPase regulation in Dahl salt-sensitive and salt-resistant rats.

Circulating Na+/K+-ATPase inhibitors have been implicated in volume-expanded forms of hypertension. Inhibition of vascular smooth muscle cell Na+/K+-ATPase has been demonstrated to elevate intracellular Ca2+ levels and enhance contractility, thus providing a mechanism of raised peripheral resistance. In cells chronically subjected to Na+/K+-ATPase inhibition, however, new Na+/K+-ATPase molecules are synthesized, which then restore the intracellular milieu to preinsult conditions. Restoral of the preinsult intracellular milieu in vascular smooth muscle cells would then be expected to lead to the reduction of muscle cell contractility and peripheral resistance. Thus circulating Na+/K+-ATPase inhibitors may not be effective in eliciting chronic forms of hypertension unless the target cell "homeostatic response" is impaired. We demonstrate an apparent such impairment in Dahl salt-sensitive rats, a genetic model of salt-sensitive hypertension.

Animals↗