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At least 415 records · Page 23Linked to original sources
PubMed2003

Chloride absorption in salt-sensitive Carrizo citrange and salt-tolerant Cleopatra mandarin citrus rootstocks is linked to water use.

In this work, seedlings of two citrus rootstocks, the salt-tolerant Cleopatra mandarin (Citrus reshni Hort. ex Tan.) and the salt-sensitive Carrizo citrange (Citrus sinensis [L.] Osb. x Poncirus trifoliata [L.] Raf.) were used to study the relationship between chloride and water uptake. The results indicated that net chloride uptake rates in both genotypes were alike and decreased linearly with the time of salinity exposure, although they were more rapidly reduced in the tolerant genotype. In each rootstock, chloride uptake rates paralleled the decreases in transpiration rates. When transpiration was modified, concomitant changes in leaf Cl(-) concentrations were observed. There was a high positive correlation between total chloride content per plant and total water absorbed. In addition, the data indicate that the tolerant genotype "excluded" more chloride, i.e. it absorbed lower amounts of chloride per volume of water. Cleopatra also possessed a less efficient root system for water uptake and a higher shoot-to-root ratio. The results show that, overall, chloride absorption is linked to water use and that further tolerance in Cleopatra is mostly conferred by superior root resistance to Cl(-) uptake. Therefore, it is proposed that chloride absorption and, hence, salt tolerance in citrus depends to a great extent upon water use.

Adaptation, Physiological↗
PubMed1999

Dietary compliance among salt-sensitive and salt-insensitive normotensive adults.

Little is known about the customary level of sodium intake by salt-sensitive people and the nature of obstacles they face in the adoption of a reduced-sodium diet. These issues were addressed with 12 salt-sensitive (SS) and 9 salt-insensitive (SI) normotensive adults. Information about sodium consumption, taste, and blood pressure and concerns about following a diet reduced in sodium were collected at baseline and monthly while participants followed a 100 mmol Na/day diet for 4 months. Mean sodium intakes of both groups were comparable at baseline and were reduced significantly during diet. The principal dietary concerns were reduced food availability, increased food costs, and reduced food palatability. There were no group differences. Ratings declined over time, but only the food palatability issue did so significantly because of a shift by the SI only. While the predictive value of SS classification remains uncertain, these data indicate that dietary change is feasible in SS subjects.

Adult↗
PubMed1988

Calcium and sodium transport in the duodenum of the Dahl salt sensitive and salt resistant rat.

We measured food intake, body growth and transport of calcium and sodium by duodenum of female Dahl salt sensitive (DS) and salt resistant (DR) rat strains. Food intake and body growth were similar for DS and DR rats taking both 0.4 and 8% sodium chloride diets. Food intake increased with age up to 5 weeks and then remained constant despite continuing body growth. Comparing DS and DR rats fed the 0.4% sodium chloride diet at 6 and 11 weeks or the 8% sodium chloride diet at 6 weeks, transport of calcium and sodium were the same in both the DS and DR groups. Transport of calcium, but not sodium, was lower at 11 than at 6 weeks. Comparing simultaneous feeding of either 0.4 or 8% sodium chloride diets to 6-week old DS and DR rat strains, transport of calcium tended to be lower in animals fed the 8% as compared to the 0.4% sodium chloride diet, and the difference was significant for net 40Ca transport for DR rats. The DS rat fed on 8% sodium chloride had higher systolic blood pressure (SBP) than the DR rat. We conclude that growing DS and DR rats, ingesting equal amounts of food, do not differ in duodenal calcium and sodium transport measured by the everted sac technique. The response to feeding sodium chloride differs between strains: the high salt diet decreases net 40Ca transport in the DR but not the DS strain.

Animals↗
PubMed1998

Mechanical properties of mesenteric resistance arteries from Dahl salt-resistant and salt-sensitive rats: role of endothelin-1.

OBJECTIVE: Hypertension has been associated with altered structure and mechanics of resistance arteries. This study assessed whether the passive mechanics of mesenteric small arteries are altered in hypertensive Dahl salt-sensitive rats (Dahl-SS) vs normotensive Dahl salt-resistant rats (Dahl-SR). The role of endothelin-1 in determining small artery mechanics was also studied. DESIGN: Male Dahl-SR and Dahl-SS were treated with high sodium (4% NaCl) for 10 weeks. Subgroups of each strain were treated with the ETA-endothelin receptor antagonist, A-127722 (30 mg/kg/d), concomitantly. Third-order branches of mesenteric arteries were mounted in a pressure myograph and exposed to intraluminal pressures ranging up to 140 mmHg. Media thickness and lumen diameter were measured at each pressure, from which wall mechanics were calculated. RESULTS: Tail-cuff systolic blood pressure was elevated with high sodium in Dahl-SS vs Dahl-SR. At the given dose, A-127722 decreased blood pressure in Dahl-SS slightly but significantly. Lumen diameter was lesser and media-lumen ratios were greater in vessels from Dahl-SS. Under isobaric conditions, vessels from Dahl-SS exhibited decreased wall stress and incremental elastic modulus. However, there were no changes in isobaric incremental distensibility or elastic modulus in relation to wall stress. A-127722 attenuated the changes in media:lumen ratio and isobaric stress observed in Dahl-SS. CONCLUSIONS: Dahl salt-sensitive hypertension was associated with altered structure of mesenteric resistance arteries, which decreased wall stress. Endothelin-1 may be involved in these changes. These arteries exhibit decreased isobaric stiffness and no difference in geometry-independent stiffness, indicating that the decreased lumen diameter is a result of eutrophic remodeling.

Animals↗
PubMed2000

Renal vascular morphology and haemodynamics in Dahl salt-sensitive rats on high salt-low potassium diet: neural and genetic influences.

OBJECTIVE: A dietary combination of high salt and low potassium (HS-LK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders Dahl salt-resistant (DR) rats hypertensive. In both strains, the hypertension is accompanied by remodelling of the renal resistance vasculature, and is attenuated by peripheral chemical sympathectomy. In the current study, we sought to determine whether the sympathetic nervous system is causally involved in mediating the renal vascular and haemodynamic alterations associated with HS-LK feeding in Dahl rats. DESIGN: Two groups each of DS and DR rats were maintained on HS-LK diet (8% NaCl, 0.2% KCl) for 8 weeks. One group of DS (n = 9) and DR (n = 8) were treated with 6-hydroxydopamine (6-OHDA) in 0.001 N HCl vehicle to chemically ablate peripheral sympathetic nerve terminals. The two remaining groups (n = 8 each) received equivalent injections of vehicle. METHODS: At the end of the dietary regimen, arterial blood pressure (ABP), glomerular filtration rate (GFR) and renal blood flow (RBF) were measured, and the structure of intra-renal resistance vessels was examined by planar morphometric analysis of coronal sections prepared from perfusion-fixed kidneys. RESULTS: Both 6-OHDA-treated and untreated DS rats presented a greater degree of intra-renal vessel remodelling characterized by reduced lumen diameter in the absence (eutrophic) or presence (hypertrophic) of cross-sectional area expansion, higher renal vascular resistance (RVR) and lower GFR and RBF than DR rats. Chemical sympathectomy increased lumen diameters and reduced vascular wall expansion, resulting in a decrease in RVR and a concomitant increase in RBF and GFR in both strains; however, the effect was more prominent in the DS rats. CONCLUSIONS: We conclude that HS-LK-induced changes in intra-renal vessel structure and renal haemodynamic function in Dahl rats are, at least in part, dependent on the activity of the sympathetic nervous system.

Animals↗
PubMed1984

Endocrine control of salt and water excretion: the role of vasopressin in DOCA-salt hypertension.

Arginine-vasopressin (AVP), the antidiuretic hormone, not only regulates water balance but may also exert direct and indirect effects on blood pressure by influencing systemic vascular resistance and body fluid volumes. Recently, specific competitive antagonists of AVP at its vascular and tubular receptors have been described. We used d(CH2)5Tyr(Me) AVP, a vascular (V1) antagonist, and d(CH2)5-D-Tyr(Et) VAVP, a vascular and tubular (V1V2) antagonist, for studies on the role of AVP in deoxycorticosterone acetate (DOCA)-salt hypertension. The antagonists were infused intravenously via osmotic minipumps in unilaterally nephrectomized rats for 6 weeks after the beginning of the DOCA-salt treatment. At the end of the experiment, blood pressure was 15 mm Hg lower in the rats receiving the V1 antagonist than in those in which the vehicle was infused. In the rats receiving the V1V2 antagonist, blood pressure was reduced by 38 mm Hg. However, these rats were in poor general condition and gained no body weight. Their plasma sodium concentration was markedly increased throughout the duration of the experiment. These results suggest that AVP contributes to the development of DOCA-salt hypertension not only through its vascular but also through its renal tubular effects. Thus AVP may act as an impormediator of volume changes associated with alterations in sodium intake or excretion and thereby affect blood pressure.

Animals↗
PubMed2003

Time-course genetic analysis of albuminuria in Dahl salt-sensitive rats on low-salt diet.

The Dahl salt-sensitive hypertensive (S) rat develops albuminuria early in life even on a low-salt diet. In contrast, the spontaneously hypertensive rat (SHR) is highly resistant to developing albuminuria despite elevated BP. An F(1) hybrid of S and SHR showed a low urinary albumin excretion (UAE) and low urinary protein excretion (UPE) similar to SHR, i.e., SHR was dominant. A genetic analysis was carried out on a large population (n = 276) obtained by backcrossing F(1) rats to the recessive S strain; the population was fed a low-salt diet. Genome scans done at 8, 12, and 16 wk of age yielded ten quantitative trait loci (QTL) for UAE and/or UPE with variable time-course patterns on nine rat chromosomes (RNO), i.e., RNO1, RNO2, RNO6, RNO8, RNO9, RNO10, RNO11, RNO13, and RNO19. There were two UPE QTL on RNO6. At most of the UAE and/or UPE QTL, the S allele was associated with increased excretion, except for one of the QTL on RNO6 and the QTL on RNO11, where the S allele caused decreased excretion. Only the UAE and UPE QTL on RNO10 co-localized with a BP QTL. The S allele on RNO10 caused higher BP and higher UAE. Two additional BP QTL were detected on RNO1 and RNO6. Most of the UAE and UPE QTL co-localized with QTL for kidney lesions characteristic of S rats. Multiple interactions were observed for UAE, many of which involved RNO2. In summary, UAE is highly polygenic and the majority of the QTL altering UAE do not co-localize with QTL for BP as evaluated by tail-cuff measurements of BP.

Albuminuria↗
PubMed1991

The k/na selectivity of a cation channel in the plasma membrane of root cells does not differ in salt-tolerant and salt-sensitive wheat species.

The characteristics of cation outward rectifier channels were studied in protoplasts from wheat root (Triticum aestivum L. and Triticum turgidum L.) cells using the patch clamp technique. The cation outward rectifier channels were voltage-dependent with a single channel conductance of 32 +/- 1 picosiemens in 100 millimolar KCl. Whole-cell currents were dominated by the activity of the cation outward rectifiers. The time- and voltage-dependence of these currents was accounted for by the summed behavior of individual channels recorded from outside-out detached patches. The K(+)/Na(+) permeability ratio of these channels was measured in a salt-sensitive and salt-tolerant genotype of wheat that differ in rates of Na(+) accumulation, using a voltage ramp protocol on protoplasts in the whole-cell configuration. Permeability ratios were calculated from shifts in reversal potentials following ion substitutions. There were no significant differences in the K(+)/Na(+) permeability ratios of these channels in root cells from either of the two genotypes tested. The permeability ratio for K(+)/Cl(-) was greater than 50:1. The K(+)/Na(+) permeability ratio averaged 30:1, which is two to four times more selective than the same type of channel in guard cells and suspension culture cells. Lowering the Ca(2+) concentration in the bath solution to 0.1 millimolar in the presence of 100 millimolar Na(+) had no significant effect on the K(+)/Na(+) permeability ratios of the channel. It seems unlikely that the mechanism of salt tolerance in wheat is based on differences in the K(+)/Na(+) selectivity of these channels.

Journal Article↗
PubMed1994

Angiotensin II induced alteration of cyclic adenosine 3',5'-monophosphate generation in the hypertrophic myocardium of Dahl salt-sensitive rat on a high-salt diet.

The objective of this study was to explore the action of angiotensin II (AII) on cardiac contractility and cyclic AMP (cAMP) generation by forskolin and isoproterenol in the hypertrophic myocardium of the salt-sensitive Dahl rat. Inbred Dahl S and Dahl R rats that had been on a diet supplemented with 6% NaCl were studied. The functional effects of the interaction of AII and forskolin on cardiac contractility were assessed in the isolated heart preparation. The effect on the cAMP signal transduction pathway was assessed in cardiomyocytes isolated from hearts of Dahl S and R rats. Dahl S rats developed cardiac hypertrophy on a high-salt diet, whereas Dahl R rats did not. Forskolin increased cardiac contractility, which was differently affected by AII, depending on whether the heart was from hypertrophied Dahl S rat or from the control Dahl R rat. AII accentuated forskolin-induced increases in cardiac contractility in hypertrophic hearts but diminished forskolin-induced increases in contractility in the nonhypertrophied hearts. This response was reflected in the cAMP response to forskolin, in that AII decreased forskolin-induced increases in cAMP in the nonhypertrophic heart. AII had the reverse effect in cardiomyocytes from hypertrophied hearts, as AII increased forskolin-induced cAMP production. This was shown to be due to an AII receptor mediated effect, as it was antagonized by the AII receptor antagonist saralasin. The same effects of AII were found on isoproterenol-induced increases in cAMP. Similar results occurred in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), suggesting that the effect was on cAMP production rather than cAMP degradation. This was attributed to an inhibitory G protein (Gi) mechanism, as the muscarinic agonist carbachol, which acts through Gi, produced the same effects as AII. Furthermore, the effects of AII were abolished by pertussis toxin, which inactivates Gi. These data indicate a reversal of control by AII in the hypertrophic Dahl S heart in response to forskolin, which activates adenylyl cyclase directly on the catalytic subunit, converting the substrate, ATP, to cAMP, independent of the guanine nucleotide activated protein, and in response to isoproterenol, which activates adenylyl cyclase through G protein mechanisms. All accentuated the forskolin-induced increase in cardiac contractility and cAMP generation in the hypertrophied ventricle but decreased both contractility and cAMP generation in nonhypertrophied hearts, suggesting that the process of cardiac hypertrophy in salt-sensitive Dahl rat may compensate for the reduction in intracellular cAMP by altering its regulatory control by AII.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Fetal bile salt metabolism: placental transfer of dihydroxy bile salts in sheep.

The bidirectional placental transfer of sodium [11,12-di-3H]chenodeoxycholate and sodium [14C]deoxycholate was studied in conscious pregnant sheep near term. In fetal-to-maternal studies, radiolabeled bile salt was injected into the fetal portal vein, and the daily excretion of radiolabel in maternal hepatic bile was measured over 3-4 days. In maternal-to-fetal studies, the mother received daily injections of radiolabeled bile salt, and the accumulation of label in the fetal pool was measured after 6-9 days. Bile salts were transferred predominantly as the taurine conjugate. Transfer rates were 1) fetus to mother; chenodeoxycholate, 6.7 mumol/24 h and deoxycholate, less than 0.5 mumol/24 h and deoxycholate, 1.4 mumol/24 h. We conclude that, in sheep near term, deoxycholate derived from the mother slowly accumulates in the fetus, while the placenta acts as an excretory route for fetal chenodeoxycholate.

Animals↗
PubMed1987

Primary resetting of left atrial sensory endings in Dahl salt-sensitive rats fed a low-salt diet.

Vagal afferent pathways contribute to vasomotor inhibition and renal sodium handling by modulating sympathetic nerve activity in rats. Low pressure or cardiopulmonary baroreflex inhibition of sympathetic nerve activity is attenuated in normotensive Dahl salt-sensitive (S) rats fed a low-salt diet. The aim of the study was to record activity in single-fiber vagal filaments from left atrial endings in Dahl S and resistant (R) rats to evaluate the mechanism for the attenuated low pressure baroreflex. Rats were fed a low-salt diet (0.1% NaCl) for 5-7 wk. Seven Dahl R and six S rats were anesthetized with urethan, and catheters were placed in the aorta and left atrium. Single-fiber recordings were obtained from the right cervical vagus. The relationship between left atrial pressure and receptor discharge was obtained during graded aortic snaring. Mean threshold for increased activation of the vagal afferents during volume expansion was 10.4 +/- 0.6 mmHg (means +/- SE) in S and 6.0 +/- 0.4 mmHg in R rats (P less than 0.002). Pressure-discharge curves were significantly shifted to the right in S rats. Maximal sensitivity of the endings expressed as delta discharge/delta LAP was not significantly different in R vs. S, but the right shift in threshold reduced the discharge of endings over a physiological range of filling pressures. We also measured left ventricular end-diastolic pressure (LVEDP) in conscious S and R rats to determine if the resetting of left atrial sensory endings could be explained by elevated left heart filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Kallikrein excretion in Dahl salt-sensitive and salt-resistant rats with native and transplanted kidneys.

Urinary kallikrein excretion is decreased in Dahl salt-sensitive (S) vs. salt-resistant (R) rats, and several lines of reasoning suggest not only that decreased kallikrein excretion is a marker for salt-sensitive hypertension but also that kallikrein might play a pathogenic role. Because previous cross-transplantation studies have demonstrated that the kidney's genotype plays a role in determining the blood pressure of the recipient in Dahl S and R rats, the present experiments were designed to determine whether both blood pressure and urinary kallikrein excretion "traveled with the kidney" in transplantation. The Rapp strains of S and R were maintained on a low- NaCl (0.13%) diet until kidney transplantation (bilaterally nephrectomized recipients), at which time the diet was switched to high NaCl (7.8%). Sixteen days later, blood pressures (tail-cuff plethysmography) of the cross-transplant groups (R/S and S/R, indicating kidney genotype/recipient genotype) were nearly identical to each other and intermediate between the blood pressures of the control groups with transplanted kidneys (R/R and S/S). Renal function studies, performed on anesthetized rats 17 days after surgery, demonstrated that R kidneys had higher glomerular filtration rates, renal plasma flows, and urinary kallikrein excretion rates than S kidneys. These differences tended to be preserved in the cross-transplant groups, and therefore they must be genetically determined intrinsic differences between R and S kidneys. This was especially striking with respect to urinary kallikrein excretion. The rank order of urinary kallikrein excretion was R/R = R/S > S/R = S/S, which implies that it is completely determined by the genotype of the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Alterations of circadian expressions of clock genes in Dahl salt-sensitive rats fed a high-salt diet.

In mammals, behavioral and physiologic processes display 24-hour rhythms that are regulated by a circadian system consisting of central and peripheral oscillators. Because various cardiovascular functions show diurnal variations and abnormal patterns of circadian blood pressure variation carry a high risk of cardiovascular complications, we investigated whether the expression of clock genes is altered in an animal model of hypertension. In Dahl salt-sensitive rats fed a high-salt (4% NaCl) diet for 6 weeks (DS-H), radiotelemetry monitoring showed increased amplitude of circadian variations in blood pressure. The ratio of heart weight to body weight and the ratio of kidney weight to body weight were higher in DS-H. Echocardiographic data showed that the wall thickness of the left ventricle was greater in DS-H. Northern blot analysis and single cosinor analysis revealed that the amplitudes of circadian expression changes of the clock genes (mPer2, Bmal1, and dbp) in the heart, liver, and kidney were significantly decreased in DS-H rats compared with a normal-salt-diet group, except for Bmal1 in the liver. The circadian expression changes of plasminogen activator inhibitor-1, a clock-regulated gene, were attenuated in the hearts of DS-H. The present results demonstrate that DS-H show altered circadian expression of peripheral clock genes. Detailed analyses of the relation between circadian expression of clock genes and blood pressure regulation might reveal a role for chronologic therapy of cardiovascular disease.

ARNTL Transcription Factors↗
PubMed2005

Reduced angiotensin II and oxidative stress contribute to impaired vasodilation in Dahl salt-sensitive rats on low-salt diet.

This study investigated the role of impaired angiotensin II (Ang II) modulation in contributing to reduced vascular relaxation in isolated middle cerebral arteries (MCA) (100 to 200 microm in diameter) of normotensive Dahl salt-sensitive (SS) rats maintained on low salt (LS) diet (0.4% NaCl) for 9 to 10 weeks. MCA from SS rats on LS diet (n=6 to 9) constricted in response to reduction of perfusate and superfusate PO2 to 35 to 40 mm Hg or acetylcholine (ACh). Vasodilator responses to reduced PO2 and ACh were restored in SS.13BN consomic rats that are 98% genetically identical to SS rats, but exhibit normal regulation of their renin-angiotensin system (RAS). This restored dilation could be prevented by feeding SS.13BN rats high-salt (HS) diet (4% NaCl) for 3 days to suppress Ang II. A continuous intravenous infusion of a subpressor dose (3 ng/kg per minute) of Ang II for 3 days restored vasodilator responses to ACh and reduced PO2 in SS.13BN rats on HS diet and in SS rats on LS diet. Superoxide scavenging with tempol (100 micromol/L) restored vasodilator responses to ACh and reduced PO2 in MCA of SS rats on LS diet, but did not affect vasodilator responses in MCA of SS.13BN rats on LS diet. These data indicate that exposure to chronically low Ang II levels leads to impaired vascular relaxation in SS rats, even when the animals are on LS diet and normotensive. This impaired relaxation appears to be mediated by increased levels of oxidative stress in the arteries.

Acetylcholine↗
PubMed2001

Renal endothelin ET(A)/ET(B) receptor imbalance differentiates salt-sensitive from salt-resistant spontaneous hypertension.

It is unclear why a subgroup of patients with essential hypertension develop salt-sensitive hypertension with progression of target organ damage over time. We evaluated the role of the renal endothelin (ET) system in the stroke-prone spontaneously hypertensive rat (SHRSP) model of salt-sensitive spontaneous hypertension (SS-SH) compared with the spontaneously hypertensive rat (SHR) model of salt-resistant spontaneous hypertension (SR-SH). Both strains were studied after either sham-operation on a normal diet (Sham) or after unilateral nephrectomy and high NaCl loading (NX-NaCl) with 4% NaCl in diet for 6 weeks (n=10, respectively). Systolic blood pressure (SBP) increased only in SHRSP-NX-NaCl compared with SHRSP-Sham (250+/-6 versus 172+/-5 mm Hg, P:<0.0001). SBP remained unchanged in SHR-NX-NaCl compared with SHR-Sham. In SHRSP-NX-NaCl animals, urinary albumin and ET-1 excretion, renal ET-1 mRNA expression, glomerulosclerosis index, and tubulointerstitial damage index were elevated compared with SHRSP-Sham (P:<0.05, respectively), whereas no significant changes were found in SHR after NX-NaCl. Urinary sodium excretion (U(Na(+))) was significantly reduced by 38% in SHRSP-NX-NaCl compared with SHR-NX-NaCl (P:<0.005, respectively). SHR animals showed a similar increase in both renal ET(A) and ET(B) receptor densities after NX-NaCl (2.2-fold, P:<0.05). In contrast, SHRSP-NX-NaCl developed a significantly more pronounced increase in ET(A) compared with ET(B) binding (4.7-fold versus 2.4-fold, P:<0.05, compared with SHRSP-Sham, respectively), resulting in a significant 2.1-fold increase in ET(A)/ET(B) receptor ratio only in the SHRSP-NX-NaCl (P:<0.05). Thus, activation of the renal ET system together with an increased ET(A)/ET(B) receptor ratio may contribute to the development and progression of SS-SH.

Albuminuria↗
PubMed1988

19-Nordeoxycorticosterone excretion in male and female inbred salt-sensitive (S/JR) and salt-resistant (R/JR) Dahl rats.

Rats were selectively bred for susceptibility (S) and resistance (R) to the hypertensinogenic effects of excess salt intake by Dahl and further inbred to virtual homozygosity by Rapp (S/JR and R/JR). The S strain has been shown to have a mutation of the cytochrome P-450-dependent 11 beta,18-hydroxylase resulting in the enhanced production of 18-hydroxydeoxycorticosterone (18-OH-DOC) compared to that of the R strain. It is known that this enzyme is also responsible for the hydroxylation of deoxycorticosterone at the 19 position to produce 19-hydroxydeoxycorticosterone. Recently, the excretion of 19-nordeoxycorticosterone (19-nor-DOC), a potent mineralocorticoid, has been shown to be markedly increased in S/JR females compared to that in R/JR females consuming a high sodium diet. While the S/JR rat is spontaneously hypertensive, the course of the disease is greatly accelerated and exacerbated by a high sodium diet. If, indeed, 19-nor-DOC is responsible for the spontaneous hypertension in the S/JR rat, then its production should also be higher in the S/JR rat consuming a normal salt diet. Furthermore, since its production is suppressed by NaCl intake, the excretion should be even higher when not suppressed by a high sodium diet. We measured the urinary excretion of 19-nor-DOC, 18-OH-DOC, and corticosterone in male and female S/JR and R/JR rats consuming a normal sodium diet. The excretions of corticosterone and 18-OH-DOC were significantly higher by S/JR of both sexes than by R/JR, with the excretion by female rats being higher than that by male rats within the same strain. The hierarchy of excretion rates of 19-nor-DOC was: S/JR females greater than R/JR females greater than S/JR males greater than R/JR male rats. These studies indicate that while S/JR rats of both sexes develop higher blood pressures than the R/JR even on a standard salt intake, the excretion of 19-nor-DOC does not correlate well with their blood pressure elevation, since the normotensive female R/JR rat excretes significantly higher quantities of 19-nor-DOC than the hypertensive male S/JR rat. Thus, it is unclear whether 19-nor-DOC is playing a significant role in the pathogenesis of the hypertension in the S/JR rat. It also remains unknown whether the renal site of formation of 19-nor-DOC allows access to the mineralocorticoid target sites in the kidney.

Animals↗
PubMed2003

Conversion of Ca2+ salt of an organic compound to its Li+ salt to simplify the fast atom bombardment mass spectrum.

The FAB mass spectrum of the Ca(2+) salt of RK-682 (1, MW 368), a potent protein tyrosine phosphatase inhibitor, shows a complex pattern due to Ca(2+) adduct ions with multimers of 1 and their decomposition ions. Addition of LiCl greatly simplified the FAB mass spectrum, providing a prominent Li(+) adduct ion of 1 at m/z 381 [M+2Li-H](+). The addition of LiCl also greatly simplified the FAB mass spectrum of calcium pantothenate. This approach may be generally useful for molecular weight determination of multivalent metal salts of organic compounds, or organic compounds that can form Li salts, by FAB mass spectrometry.

Calcium↗
PubMed1996

Inaccuracy of three-finger pinch method of determining salt content in homemade sugar salt solutions.

Oral rehydration therapy (ORT) has dramatically reduced the morbidity and mortality associated with acute infectious diarrhea. Commercial oral rehydration salt (ORS) solutions with sodium concentrations of 30-90 mmol/L are ideal for both the prevention and treatment of dehydration. However, logistic issues impede their universal availability and homemade sugar salt (HSS) solutions are widely used in some areas of the world. The least accurate methods of preparing HSS solutions utilize a three-finger pinch of salt. The present study demonstrates the inconsistency and inaccuracy of this method among 15 health workers who participated in an ORT training seminar conducted in a situation that approximated field conditions. Similar studies with different subjects, instructions, and milieu describe results similar to those we obtained. In all studies, including the present one, a substantial number of the solutions prepared by this method had dangerously high or low sodium concentrations. Health providers should consider the use of selected home-available fluids rather than HSS solutions for the prevention of dehydration in children with diarrhea. However, ORS solutions should be used to correct established dehydration.

Adult↗