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At least 19 recordsLinked to original sources

PubMed1992

High salt diet down-regulates proximal tubule Na+, K(+)-ATPase activity in Dahl salt-resistant but not in Dahl salt-sensitive rats: evidence of defective dopamine regulation.

We examined the regulation of Na+,K(+)-ATPase activity in proximal tubule segments during a high salt diet in prehypertensive Dahl salt-sensitive and salt-resistant rats. Rats were placed on normal salt or high salt diets (0.9% saline as drinking water). During the normal salt diet, Na+,K(+)-ATPase activity was not different between Dahl salt-sensitive and salt-resistant rats. After 2 days and 10 days on a high salt diet, Na+,K(+)-ATPase activity in Dahl salt-resistant rats significantly decreased when compared to Dahl salt-resistant rats on a normal salt diet (P less than 0.01). The decreased Na+,K(+)-ATPase activity in Dahl salt-resistant rats during a high salt diet was reversed by treatment with an inhibitor of aromatic L-amino acid decarboxylase (dopamine synthesizing enzyme), benserazide. In contrast, Na+,K(+)-ATPase activity did not decrease during the high salt diet and benserazide had no effect on Na+,K(+)-ATPase activity in Dahl salt-sensitive rats. These results indicate that Dahl salt-sensitive rats do not have the capacity to down-regulate the proximal tubule Na+,K(+)-ATPase activity during a high salt diet. Indirect evidence suggests that the regulation of Na+,K(+)-ATPase activity by locally produced dopamine is absent in Dahl salt-sensitive rats.

Animals↗

PubMed1992

Preferred salt levels and salt taste acuity in human subjects after ingestion of untasted salt.

We have examined whether salt loading alters the salt preference or salt taste acuity of nine human subjects on continuous low salt diet. Subjects were randomly assigned to either untasted salt tablets (120 mmol/day) or placebo over a 2-week period at the end of which salt preference and salt recognition thresholds were measured. Subjects then received the alternate substance for another 2 weeks and the measurements were repeated. While urinary Na+ and Cl- were significantly increased while on salt tablets, urinary volume, K+, urea and creatinine concentrations, blood pressure, body weight, salivary and plasma electrolyte concentrations were unchanged. Plasma renin and aldosterone levels were reduced while on salt tablets but not significantly. Salt tablets caused a significant increase in sodium recognition threshold but a significant decrease in salt addition to unsalted tomato juice and in ideal salt level assessed by presalted (150 mmol/l) tomato juice. Thus, an increase in untasted dietary salt may reduce salt preference in human subjects, a finding opposite to that with an increased, tasted salt intake over a similar period.

Adult↗

PubMed1992

The Salt Step Test: its usage in the diagnosis of salt-sensitive hypertension and in the detection of the salt hypertension threshold.

The Salt Step Test was devised to characterize the response of the hypertensive patient to dietary salt. The test has three phases: unrestricted salt, to document hypertension and customary salt intake; restricted salt (2 g/day), to identify the salt-sensitive patient; and stepwise increased salt (each step = 1 g/day), to find the level that precipitates hypertension. The Salt Step Test identified that out of 30 well-established adult hypertensives, 13 were salt-sensitive. It also revealed that in each salt-sensitive patient, a distinct level of salt (range 3-16 g/day) precipitated hypertension, i.e., a Salt Hypertension Threshold. Definition of the Salt Hypertension Threshold should be useful in providing specific, individualized guidelines for dietary salt restriction.

Adult↗

PubMed2026

Identification and analysis of HD-ZIP transcription factors that regulate salt gland development and salt tolerance in Limonium bicolor.

Soil salinity severely constrains agricultural production. Elucidating the salt-tolerance mechanisms of halophytes can provide innovative approaches for improving the salt tolerance of crop plants. In this study, we performed genome-wide identification and analysis of 36 LbHDZ genes encoding homeodomain-leucine zipper (HD-ZIP) transcription factors in Limonium bicolor, a typical recretohalophyte that excretes excess salt ions through specialized salt glands. Expression profiling across different stages of salt gland development, as well as in various tissues under salt stress, indicated that multiple LbHDZ genes are involved in regulating salt gland development and salt tolerance. Among these genes, LbHDZ14 (a member of the HD-ZIP II subfamily) exhibited sustained high expression during the critical period of salt gland formation, while its transcript levels were significantly downregulated in leaves and roots under salt stress. Subsequent experiments demonstrated that LbHDZ14 is localized in the nucleus and negatively regulates salt gland density and salt tolerance by directly binding to the promoter of LbGDSL, a positive regulator of salt gland development. In conclusion, this study reveals the expression patterns of LbHDZ genes in L. bicolor, characterizes the functional mechanism of LbHDZ14, further elucidates the regulatory network underlying salt gland development, and provides candidate genes for enhancing crop salt tolerance.

Plumbaginaceae↗

PubMed2026

Transcription factor LbUBC positively regulates salt gland development and salt tolerance by directly binding to the LbTTG1 promoter and repressing its transcription.

KEY MESSAGE：: LbUBC enhances salt tolerance by promoting salt gland development via repressing LbTTG1, revealing a synergisticregulatory mechanism in Limonium bicolor. In the context of increasingly severe soil salinization, salt-tolerant genetic resources from halophytes show great application potential. In particular, the recretohalophyte Limonium bicolor, which possesses specialized salt gland structures, has become a key model for deciphering the molecular mechanisms underlying salt tolerance and salt gland development. In this study, using LbTTG1-overexpressing and -silenced lines, we demonstrate that LbTTG1 negatively regulates salt-gland development and salt tolerance. Through yeast one-hybrid, EMSA, and dual-luciferase assays, Lb7G33228 (LbUBC) was screened and verified as an upstream transcriptional regulator of LbTTG1. LbUBC enhances salt tolerance in L. bicolor by positively regulating salt-gland development, verified using LbUBC silence and overexpression strains. Interestingly, LbUBC represses the expression of its downstream target LbTTG1, thereby releasing the inhibitory effect of LbTTG1 on salt-gland development. In this manner, LbUBC positively regulates salt-gland development, achieving a dynamic balance in the regulation of salt-gland development and salt tolerance in L. bicolor. This study reveals a synergistic regulatory mechanism involving multiple genes, offering new insights for comprehensively dissecting the molecular regulatory network of salt-gland development.

Salt Tolerance↗

PubMed1992

Effects of sodium salts on pressor reactivity in salt-sensitive men.

Blood pressure in patients with essential hypertension is raised by sodium chloride but not by nonchloride sodium salts. Although a high sodium chloride diet is known to augment the pressor response to norepinephrine and angiotensin II, the effect of nonchloride sodium salts on pressor responsiveness has not been studied so far. To examine whether sodium chloride and nonchloride sodium salts evoke different pressor responses to these agonists, we performed graded norepinephrine and angiotensin II infusions in salt-sensitive (n = 7) and salt-resistant (n = 8) normotensive subjects. The subjects were given a low salt diet (20 mmol/day) for 3 weeks, to which a supplement of 200 mmol sodium per day, provided as either sodium chloride or sodium citrate, or a placebo was added for 1 week each. We found that, although sodium chloride raised mean arterial blood pressure in the salt-sensitive subjects (p less than 0.005), sodium citrate did not. However, under both sodium salts pressor response to norepinephrine and angiotensin II was significantly greater than under placebo (p less than 0.02). Furthermore, with both sodium salts, pressor response in the salt-sensitive subjects was greater than in the salt-resistant subjects (p less than 0.01). This study thus demonstrates that, although blood pressure in salt-sensitive individuals is raised by sodium chloride only, both sodium chloride and sodium citrate evoke similar increases in pressor response to norepinephrine and angiotensin II. Since pressor response increased with both sodium salts but resting blood pressure increased only with sodium chloride, enhanced pressor responsiveness alone cannot account for the sodium chloride-induced rise in resting blood pressure.

Adult↗

PubMed1975

Interactions of cationic bile salt derivatives with the ileal bile salt transport system.

Previous structure-activity studies of the active ileal bile salt transport system have demonstrated that a single negative charge on the side chain is essential for active transport. Furthermore, mutual inhibition studies between different pairs of bile salt substrates indicated that dihydroxy bile salts had a greater apparent affinity for the transport system than the trihydroxylated compounds and triketo bile salts had the least such affinity. In this study, a series of cationic bile salt derivatives (cholamine conjugates) were prepared with one, two, and three alpha-hydroxyl groups on the steroid moiety. Based on the previous observations one would expect (1) no active transport of any of the cholamine conjugates by the ileal transport system; (2) interaction of these compounds with the transport system in such a way as to inhibit the transport of bile salts, with inhibition potency of the transport of any single bile salt inversely related to the number of hydroxyl groups present on the cholamine conjugate; and (3) transport of triketo anionic bile salts to be most readily inhibited, trihydroxy compounds less readily inhibited, and dihydroxy bile salts least inhibited. Using everted gut sac preparations it was demonstrated that all three aforementioned expectations did occur. Furthermore, reversible inhibition of ileal absorption of taurocholate and the bile salt derivative taurodehydrocholate could be demonstrated in vivo. The dihydroxy cholamine conjugates were better inhibitors than the trihydroxy compound. Relative specificity for the bile salt system of these cationic bile salt derivatives was demonstrated in the in vivo preparation by comparing its inhibition of taurodehydrocholate absorption with their lesser capacity to inhibit glucose transport.

Animals↗

PubMed1979

Regulation of hepatic transport of bile salt. Effect of protein synthesis inhibition on excretion of bile salts and their binding to liver surface membrane fractions.

The overall transport of bile salts across the hepatocyte is characterized as a carrier-mediated process whose rate-limiting step is biliary secretion. Specific bile salt binding proteins have been identified in liver surface membrane fractions and were postulated to represent the initial interaction in bile salt translocation across both the sinusoidal and canalicular membranes. To test this hypothesis, cycloheximide was administered to rats to inhibit hepatic protein synthesis. 16 h after cycloheximide administration [14C]leucine incorporation into hepatic protein was inhibited by 93% at 1 h and 47% at 12 h. However, values of liver function tests were not increased, although serum albumin, serum alanine amino-transferase, and alkaline phosphatase were significantly decreased. Light and electron microscopy did not demonstrate necrosis or fat accumulation. The latter demonstrated minimal disorganization of rough endoplasmic reticulum and occasional lamellar whorls. 16 h after cycloheximide administration bile salt independent bile flow, basal bile salt excretion, and basal bile flow were unaltered, but the maximum bile salt transport capacity was reduced to 62% of control and 24 h later to 38%. Decreased bile salt transport was reversible, for it returned to control values after 48 h, when hepatic protein synthesis was also normal. Maximum bromosulfophthalein (BSP) transport, on the other hand, was reduced after 16 h to only 85% of control. Both bile salt and BPS maximum transport capacities decreased with time during inhibition of protein synthesis, apparently following first order kinetics. It was estimated that their half-lives are 20 h for bile salt transport and 55 h for BSP transport. These different turnover rates suggest that cycloheximide does not decrease active transport through generalized hepatic dysfunction or alteration of high energy sources possibly required for transport. The maximum number of [14C]cholic acid binding sites in liver surface membrane fractions was determined by an ultrafiltration assay. They were reduced to 68% of control after 16 h of cycloheximide and to 25% after 24 h. This reduction in the number of binding sites is apparently selective, for the activities of the liver surface membrane enzymes (Na+-K+)ATPase, Mg++-ATPase, and 5'-nucleotidase were not significantly changed. The associated alterations in bile salt transport and the maximum number of binding sites after cycloheximide administration suggests that these receptors may be the bile salt carriers.

Animals↗

PubMed1977

Bile salt metabolism. II. Bile salts and disease.

Alterations of bile salt metabolism have been shown in numerous diseases. Liver damage results in elevated serum bile salt concentrations which may be useful as a sensitive index of hepatocellular disease. Changes in the relative proportions of the individual bile salts in serum occur with cholestasis. Urinary excretion of bile salts, largely in the form of sulphates, increases as a compensatory mechanism. Ileal disease or resection causes bile salt melabsorption. The increase in colonic bile salts produces a watery diarrhoea while the decrease in duodenal levels may cause steatorrhoea. Cholelithiasis may result from alteration in the relative proportions of cholesterol, lecithin and bile salts in bile. The mechanism apparently differs in various conditions predisposing to gallstone formation. A primary alteration of bile salt metabolism has been postulated in several other conditions. Considerable interest centres on the importance of metabolites of bile salts in the pathogenesis of colonic carcinoma. Chenodeoxycholic acid is a successful though costly treatment for selected patients with cholesterol gallstones. Bile salt binding agents, such as cholestyramine, are extremely useful especially in the control of pruritus in patients with cholestasis.

Animals↗

PubMed1992

Sodium and noradrenaline in cerebrospinal fluid and blood in salt-sensitive and non-salt-sensitive essential hypertension.

1. The effects of dietary sodium on blood pressure and levels of sodium, other electrolytes and noradrenaline (NA) in the cerebrospinal fluid (CSF) and blood of 15 patients with essential hypertension were studied. The CSF and blood sampling was carried out after 7 days of a high salt intake (16-18 g/day) and after 7 days of a low salt intake (1-3 g/day). 2. Blood pressure and sodium concentrations in CSF and serum were significantly higher in the high salt period than the low salt period (CSF Na+ concentration: 147.7 +/- 0.4 mmol/L vs 145.3 +/- 0.5 mmol/L; P less than 0.001). Levels of CSF pressure and potassium or calcium concentrations were not different between the two periods. Plasma NA and plasma renin activity (PRA) were lower and CSF NA levels tended to be lower in the high salt period. 3. The levels and the changes in sodium and NA in CSF were not significantly different between the salt-sensitive (n = 8) and the non-salt-sensitive (n = 7) subjects, but the changes in plasma NA and PRA were smaller in the salt-sensitive subjects. 4. These results indicate that the sympathetic nervous system is less suppressed in salt-sensitive subjects during high salt intake. This may be due to altered neural responsiveness to sodium loading rather than being greater increases in sodium concentration in the central nervous system.

Adult↗

PubMed1992

Sodium kinetics in salt-sensitive and salt-resistant normotensive and hypertensive subjects.

OBJECTIVE: To test the hypotheses that sodium kinetics are not affected by blood pressure, salt sensitivity, salt resistance or race, and that the kinetics of sodium balance are not a first-order process. DESIGN, PARTICIPANTS AND INTERVENTIONS: Two studies were conducted. In the first, 18 normotensive and 36 hypertensive men and women were given sodium at 120 mmol/day for 6 days, followed by 10 mmol/day for 8 days, then 400 mmol/day for 8 more days. Salt sensitivity was defined as an increase in diastolic blood pressure from the 10 to the 400 mmol/day intake. Salt resistance was defined as no increase, or a decrease in diastolic blood pressure with the increased sodium intake. In the second study, 12 white and 12 black normotensive men ingested sodium at 10, 200 or 400 mmol/day in random order, each for 7 days. All urine was collected in both protocols. SETTING: Metabolic ward at the University of Greifswald (Greifswald, Germany; study 1), and Clinical Research Center (Indiana University, Indianapolis, Indiana, USA; study 2). MAIN OUTCOME MEASURE: In addition to conventional statistics, a pharmacokinetic analysis was carried out to determine the elimination rate constant and half-life. RESULTS: In the Greifswald study, when the sodium intake was decreased, a longer half-life was determined for the salt-sensitive than the salt-resistant hypertensive subjects. The half-life for the normotensive salt-sensitive and salt-resistant subjects did not differ. When the sodium intake was decreased, a monoexponential equation fitted the data for all subjects; when the sodium intake was increased, only data for half the subjects could be fitted to the same equation. In the Indianapolis study, black race had a significant influence upon urinary sodium excretion. Furthermore, the half-life for sodium elimination was dependent upon sodium intake; namely, the greater the intake, the longer the elimination half-life. CONCLUSIONS: The time required to reach sodium balance may increase following salt-sensitive increases in blood pressure rather than precede them. Race influences the time required to achieve salt balance. Sodium kinetics are not a first-order process.

Adult↗

PubMed1977

Effect of sugars on salt reception in true slime mold Physarum polycephalum. Physicochemical interpretation of interaction between salt and sugar receptions.

Interaction between salt and sugar receptions in plasmodium of Physarum polycephalum was studied by using double-chamber method. Effect of sugars on salt reception was evaluated by measuring membrane potential and the motive force of tactic movement of the slime mold, where salt concentration in one compartment was increased successively with a fixed sugar concentration. Results are summarized as follows: (1) The presence of D-glucose, D-mannose, D-maltose, or sucrose in medium led to increase of the threshold concentration Cth, for salts (chlorides and nitrates of Li, Na, K), whereas D-ribose decreased the threshold for salt reception. D-galactose showed no appreciable effect on Cth of every salt species examined. No change in Cth for salt reception was observed until concentration of sugars exceeded their respective thresholds. (2) Double logarithmic plots of Cth for salts against sugar concentration followed different straight lines for different cations, whose slopes being closely correlated with the effects of lyotropic number of anions in the absence of sugars. (3) Plots of log Cth against the reciprocal of the absolute temperature, 1/T, gave linear relations, and the slopes of the straight line became small with increase of sugar concentration above their respective thresholds. Experimental results obtained here suggest that the structure of water at the interface of cell membrane plays an indispensable role in the interaction between salt and sugar receptions.

Anions↗

PubMed1992

Higher salt consumption, digoxin-like factor, and nifedipine response are associated with salt sensitivity in essential hypertension.

In addition to demonstrating evidences of increased sympathetic nervous system activity and marked left ventricular hypertrophy in salt-sensitive hypertensives, our group has also reported increased weight gain with salt overload in these patients. The increased weight gain suggests volume expansion, a situation already shown to increase plasma levels of a Na, K-ATPase inhibitor. Therefore, in the present study, digoxin-like factor (DLF) serum levels, spontaneous salt ingestion, nifedipine hypotensive effect, and plasma renin activity were evaluated in essential hypertensive subjects. Thirteen essential hypertensive outpatients were studied sequentially on an ad lib diet, a low salt diet (LSD = 30 mEq Na/day), and a high salt diet (HSD = LSD + 171 mmol/L NaCl/day), 1 week each. On the seventh day of LSD and HSD, DLF levels, mean blood pressure (MBP) response to nifedipine (10 mg sublingual), and plasma renin activity were measured. The MBP percent change from the seventh day of LSD to the seventh day of HSD (salt sensitivity) ranged from -13.7 to 20.9%. A positive correlation (r = 0.64, P < .01) was observed between salt sensitivity and 24-h urinary sodium excretion with an ad lib diet. The DLF serum levels correlated with the salt sensitivity both on LSD (r = 0.50, P < .05) and on HSD (r = 0.53, P < .05). Salt sensitivity was positively correlated with the difference of response to nifedipine between HSD and LSD (r = 0.78, P < .001). Plasma renin activity correlated inversely with DLF on LSD (r = -0.51, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

High sucrose diets increase blood pressure of both salt-sensitive and salt-resistant rats.

We examined the effects of a diet relatively high in sugar and low in protein content on systolic blood pressure (SBP) in rats with known pressure responses to salt (NaCl) in order to compare "sugar/protein sensitivity" to "salt sensitivity." Dahl salt-sensitive (DSS) and salt-resistant (DSR) rats were fed one of two low salt diets containing either high sugar (sucrose 51.5% w/w)/low protein (14.6% w/w) or low sugar (sucrose 12.5% w/w)/high protein (52.2% w/w) content. After 3 weeks, the DSS ingesting the high sugar diet/low protein diet developed significantly elevated SBP relative to DSR eating the same high sugar/low protein diet and the DSS and DSR consuming the low sugar/high protein diet. After 2 to 3 months, the SBP of DSR eating the high sugar diet began to rise markedly and eventually both DSS and DSR ingesting the high sugar/low protein diet maintained similarly elevated SBP, significantly higher than DSS and DSR ingesting the low sugar/high protein diet. When Fischer 344 rats, a normotensive, salt-resistant rat strain, were fed the high sucrose/low protein diet, SBP also rose significantly into hypertensive ranges over 2 to 3 months. Since the SBP of DSR and Fischer 344 rats are not influenced to any great extent by high salt intake, even after prolonged exposure, the SBP rise associated with the high sugar/low protein diet may be via a mechanism different from salt-induced hypertension. However, it is also possible that the high sugar/low protein diet creates in DSS and DSR the situation responsible for salt induction in DSS.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1992

Blood pressure response to hyperinsulinemia in salt-sensitive and salt-resistant rats.

We investigated the role of insulin in salt-sensitive hypertension in Dahl salt-sensitive and salt-resistant rats. The rats were kept in metabolic cages, and sodium intake and urinary sodium excretion were measured. In salt-sensitive rats receiving a 0.3% NaCl diet, sodium retention was significantly greater at weeks 1 and 2 in rats that received an insulin infusion than in those receiving a saline infusion. Mean arterial blood pressure and plasma norepinephrine levels were significantly higher at week 3 in insulin-treated rats than in saline-treated rats (mean arterial pressure, 137 +/- 3 mm Hg versus 119 +/- 3 mm Hg, p < 0.05; plasma norepinephrine, 0.40 +/- 0.02 ng/ml versus 0.27 +/- 0.01 ng/ml, p < 0.05). Insulin did not influence sodium retention, mean arterial pressure, or plasma norepinephrine in salt-resistant rats. Coadministration of an alpha-blocker (bunazosin, 10 mg/kg per day for 3 weeks) in salt-sensitive rats abolished the insulin-induced elevations in mean arterial pressure and sodium retention. When salt-sensitive rats were fed a low salt diet (0.03% NaCl), insulin did not raise mean arterial pressure. Thus, insulin elevated blood pressure only in the salt-sensitive model. The sympathetic nervous system and sodium retention in the early phase of insulin overload may contribute to elevation of mean arterial pressure in this model.

Animals↗

PubMed1978

Histochemical enzyme activity correlated to the structural segmentation of the proximal convoluted tubule in salt-depleted and salt-loaded rat kidneys.

In salt-depleted and salt-loaded rat kidneys a study was made of the structural segmentation of the proximal convoluted tubule (PCT) and the histochemical activity of non-specific acid and alkaline phosphatases and succinate dehydrogenase in the same segments. No quantitative structural or segmental alterations were observed, but significant changes in enzyme activity occured. These comprised: 1) A decrease in activity of acid phosphatase in segment 1 and the transitional zone in salt-depleted kidneys, and an increase in enzyme activity in segment 2 in salt-loaded kidneys. 2) a decrease in alkaline phosphatase activity in segment 2 in both salt-depleted and salt-loaded kidneys and 3) a decrease in succinate dehydrogenase activity in segment 2 in salt-depleted kidneys, and an increase in activity in the same segment in salt-loaded kidneys. Thus long-term variation in sodium intake are followed by segment-correlated variations in the activity of acid and alkaline phosphatase and succinate dehydrogenase in the PCT.

Acid Phosphatase↗

PubMed1976

Blood pressure, salt preference, salt threshold, and relative weight.

This study was performed to observe the relationships of salt preference, salt threshold, the relative weight to blood pressure. Three groups were selected from 4,800 school children on the basis of mean blood pressure: less than or equal to fifth percentile, in the area of the 50th percentile, and greater than or equal to 95th percentile. Salt threshold was determined by titrating, on each subject's tongue, solutions ranging from 1 to 60 millimols/liter of sodium chloride. Salt preference was tested by the addition of salt by each subject to unsalted tomato juice and beef broth according to individual taste. The samples were then analyzed for sodium concentration. The coefficient of correlation for the amount of salt added to juice and broth was significant (r=0.63). There was no relationship of salt threshold to preference, nor did threshold or preference relate to blood pressure. Relative weight was related to blood pressure range being the most obese.

Adolescent↗

PubMed1979

The effect of angiotensin-converting enzyme inhibition on regional blood flow in salt-depleted and salt-loaded normotensive conscious rats.

The effect of angiotensin-converting enzyme inhibition on regional blood flow was studied in a total of 21 normotensive Wistar rats fed on either low or high salt diet. A new potent angiotensin-converting enzyme inhibitor (CEI), SQ 14,225 was administered intravenously in a dose of 2 mg/Kg to the conscious animals, and changes in fractional distribution of cardiac output were determined with a microsphere method. Prior to administration of CEI, there was no significant difference in mean arterial pressure (MAP) or regional blood flow between salt-depleted and salt-loaded rats. With CEI, MAP did not change significantly in either group. Fractional distribution of cardiac output increased to the kidneys (p less than 0.002), and decreased to the stomach, spleen, and skeletal muscle (p less than 0.02, p less than 0.002, and p less than 0.01, respectively) in the salt-depleted group, while a pattern of blood flow distribution was not changed in the salt-loaded group. These results suggest that angiotensin II plays an important role in regulating regional blood flow in salt-depleted conscious animals, but not in salt-loaded ones.

Angiotensin-Converting Enzyme Inhibitors↗