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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↗

PubMed1989

Various sodium salts, potassium salts, a calcium salt and an ammonium salt induced ornithine decarboxylase and stimulated DNA synthesis in rat stomach mucosa.

Studies were made on the possible tumor-promoting activities of various salts of food additives in the glandular stomach mucosa of F344 male rats after their administration by gastric intubation. Up to 100-fold increases in ornithine decarboxylase (ODC) activity in the pyloric mucosa of the stomach with maxima after 8 h were observed after administration of sodium acetate at doses of 3.68-13.6 mmol/kg body weight, sodium L-ascorbate at doses of 8.55-17.1 mmol/kg body weight, Na2CO3 at doses of 4.73-14.2 mmol/kg body weight, sodium L-glutamate at doses of 12.8-17.1 mmol/kg body weight, sodium sorbate at doses of 8.92-17.1 mmol/kg body weight and (NH4)2SO4 at doses of 7.56-20.1 mmol/kg body weight. Increases of up to 100-fold in ODC activity with maxima after 16 h were also observed after intubation of KCl at doses of 10.1-22.0 mmol/kg body weight, K2SO3 at doses of 2.84-8.45 mmol/kg body weight, K2S2O5 at doses of 2.25-6.75 mmol/kg body weight and CaCl2 at doses of 2.0-4.08 mmol/kg body weight. Sodium acetate at a dose of 11.0 mmol/kg body weight, KCl at a dose of 20.1 mmol/kg body weight, K2S2O5 at a dose of 5.40 mmol/kg body weight and CaCl2 at a dose of 3.4 mmol/kg body weight induced up to 10-fold increase in DNA synthesis in the pyloric mucosa of the stomach with maxima after 16-24 h. These results suggest that these salts of food additives may, like NaCl, have tumor-promoting activities in the pyloric mucosa of rat stomach.

Animals↗

PubMed1987

Effects of salt loading on the fractional volume of atria-specific granules in Dahl salt-sensitive and salt-resistant rats.

The cardiac atria are known to play a role in blood volume homeostasis, secreting a peptide that induces a potent natriuresis and diuresis. This peptide is atrial natriuretic factor (ANF), and its primary site of storage is within atria-specific granules found in atrial cardiocytes. Since salt loading results in an increase in circulating levels of ANF, our aim was to determine if the atria-specific granule population in the cardiocytes of Dahl rats would decrease accordingly. To this end, the fractional volume of the atria-specific granules was determined by ultrastructural morphometric analysis in the Dahl salt model of hypertension. This analysis was performed on the right atria of Dahl Salt-resistant (DR) and salt-sensitive (DS) rats fed either a low-salt (0.4%) or high-salt (8%) diet for 12 weeks prior to sacrifice. DR and DS rats fed a low-salt diet had significantly reduced plasma sodium levels and osmolalities, and a significantly lower mean arterial blood pressure than did rats fed a high-salt diet. The fractional volume of atria-specific granules was significantly lower in salt-loaded DR (P less than 0.01) and DS (P less than 0.025) rats than in their respective low-salt controls. This significant decrease in atrial granules corresponds to the reported decrease in the storage of atrial ANF in salt-loaded rats, and provides a morphological verification of the biochemical studies. Moreover, these results, in combination with a growing body of physiological data, lend support to the hypothesized role of ANF in the regulation of water-electrolyte balance, which may play an important role in cardiovascular pathophysiological states related to hypertension.

Animals↗

PubMed1990

Salt intake and renal hemodynamics in immature and mature Dahl salt-sensitive (DS/JR) and salt-resistant (DR/JR) rats.

To determine if abnormalities in the maturation of renal function in Dahl salt-sensitive rats are associated with the development of hypertension, studies were performed in anesthetized 3 week old salt-sensitive (DS/JR) and salt-resistant (DR/JR) rats whose mothers were maintained on 0.15% (low-salt) during gestation and either 0.15% or 2.0% (high-salt) NaC1 diets after parturition. Mature DS/JR and DR/JR rats were maintained on either 0.15% or 2.0% NaC1 diets after weaning and studied at 8 to 9 weeks of age. High-salt diet raised blood pressure (BP) and reduced glomerular filtration rate (GFR) and renal blood flow (RBF) in mature DS/JR rats, but had no effect on BP, GFR and RBF in mature DR/JR rats. In immature DS/JR and DR/JR animals, high-salt intake resulted in poor growth with reductions in GFR and RBF in the DS/JR group. The response to acute volume expansion, (5% body weight physiologic saline infusion) differed among the groups. Mature rats all vasodilated while immature high-salt DS/JR did not, and immature low-salt DS/JR vasoconstricted. These studies demonstrated that both mature and immature DS/JR rats evidence abnormal responses to acute and chronic salt loading. Early exposure to high-salt intake affects the maturation of renal function in the DS/JR group. An enhanced vascular sensitivity to sodium is present at critical periods of postnatal development in DS/JR rats.

Animals↗

PubMed1989

Differential effect of dietary salt on renal growth in Dahl salt-sensitive and salt-resistant rats.

A high salt diet has been shown to increase renal mass of intact rats, although the mechanism by which this occurs has not been investigated. We used Dahl rats that are sensitive (DS) or resistant (DR) to the hypertensinogenic effect of salt to examine changes in renal size and composition caused by a high salt diet. Renal index, deoxyribonucleic acid (DNA), protein, water content, protein/DNA ratio, and cell number and size were measured in age-matched DR and DS on a high salt diet for 7, 14, or 28 days. The results were compared with those obtained from respective rats on a low salt diet. High salt diet elevated renal index and protein in DR and DS rats at each time point. After 7 days of a high salt diet, DNA increased in DS only. Protein/DNA ratio was progressively decreased by a high salt diet in DS and remained unchanged in DR rats. Cell number was increased 35% in DS versus only 13% in DR rats at 4 weeks. Cell size decreased 24% in DS and only 11% in DR rats. These results indicate that renal growth due to hyperplasia accompanies ingestion of a high salt diet in both DR and DS rats, but the rate of growth and the mechanism through which it occurs differ between strains. This difference may be important in delineating salt sensitivity and future development of hypertension.

Animals↗

PubMed1988

Genetic influences on the response to dietary salt reduction, acute salt loading, or salt depletion in humans.

The effect of heredity on blood pressure is established. However, not all genetically predisposed individuals develop an elevated blood pressure. Thus, an environmental factor may also be required for expression of this genetic predisposition. To elucidate this effect further, as well as to examine the relationship between inherited factors and the influence of salt intake, we conducted acute and chronic investigations in normal subjects. We present evidence that renal function, the renin-angiotensin-aldosterone system, and sympathetic nervous system are all influenced by genetic variance. We found that the blood pressure response to both acute changes in volume and changes in salt intake is normally distributed, supporting the notion of salt sensitivity and resistance of blood pressure. We identified phenotypes of haptoglobin as possibly useful indicators of salt sensitivity and resistance. We documented a parent-offspring resemblance in blood pressure and also a maternal-offspring resemblance in the change in blood pressure with salt reduction. We present evidence that suggests that salt-sensitive persons exhibit differences in renin-aldosterone relationships and natriuretic responses consistent with volume expansion compared to salt-resistant individuals. Finally, we identified a potential role for altered adrenoreceptors in the development of salt sensitivity. Our observations speak to the inherited nature of salt sensitivity and resistance of blood pressure. They may have mechanistic implications as well.

Diet, Sodium-Restricted↗

PubMed1989

Morphometric evaluation of the renal arterial system of Dahl salt-sensitive and salt-resistant rats on a high salt diet. II. Interlobular arteries and intralobular arterioles.

The progression of small vessel renal vascular disease was studied in inbred Dahl salt-sensitive (SS/Jr) and salt-resistant rats with acute hypertension induced by a high salt diet. Corrected cross-sectional areas of wall (WAC) and lumen were measured by planimetry and histologic staining for fibrin, hyalin deposition, and elastic lamellae was performed. In SS/Jr rats on the high salt diet, the hallmarks of malignant hypertension (fibrinoid necrosis, hyperplastic and necrotizing arteritis) appeared by week 2 and were intensified after 4 weeks on the high salt diet. Renal vascular lesions from SS/Jr rats were characterized by: hyperplasia and/or hypertrophy of medial smooth muscle cells; intimal proliferation; fibrin, basophilic mucoid, and hyalin deposition within the the subendothelial space and media; variable adventitial fibrosis; and accumulation of mononuclear inflammatory cells in the adventitia and media. Interlobular arteries from both rat strains exhibited significantly increased cross-sectional areas over time for all measured parameters. Intralobular arterioles from both rat strains exhibited significantly increased cross-sectional areas over time for all measured parameters except lumen from SS/Jr rats. For SS/Jr rats, increased WAC from both arterial divisions correlated positively with systolic blood pressure, but not body weight. In salt-resistant rats, increased WAC from both arterial divisions correlated positively with body weight, but not systolic blood pressure. We concluded that the rapid increase in WAC from SS/Jr rats could not be attributed solely to the normal growth of the rat. With the development of acute hypertension in the SS/Jr rat, these results demonstrate the potential usefulness of this model to investigate the pathogenesis of similar renal vascular alterations which are observed in man.

Analysis of Variance↗

PubMed1986

Genetic and salt-related alterations in monoamine neurotransmitters in Dahl salt-sensitive and salt-resistant rats.

Monoamine and metabolite levels were determined in brain regions and in the kidney, heart and adrenals taken from Dahl salt-sensitive (DS) and salt-resistant (DR) rats on either normal (NS) or high (HS) (8.5% NaCl) salt diets. The HS diet significantly (p less than 0.01) elevated blood pressure only in DS rats. DS-HS rats had a significantly (p less than 0.001) greater increase in renal weight and a significantly (p less than 0.001) greater reductions in renal norepinephrine (NE) content and concentration than the DR-HS rats. Cardiac NE content and concentration were also lower (p less than 0.001) in DS rats when compared to DR rats. Adrenal catecholamines were also altered in DS rats. There were genetic differences in brain regional levels of NE, dopamine (DA) and serotonin (5-HT) between DR and DS rats. NE levels were significantly (p less than 0.03) higher in DS compared to DR rats in the pons and hypothalamus. DA levels were significantly (p less than 0.01) greater in the striatum of DS compared to DR rats as were 5-HT levels in the striatum and cortex. HS diets had no effect on brain monoamine or metabolite levels in either DS or DR rats except to elevate cortical 5-hydroxyindoleacetic acid levels. The cardiovascular implications of these genetic and salt-related changes in peripheral and central nervous system monoamines were discussed.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1991

Salt-induced plasticity in cardiopulmonary baroreceptor reflexes in salt-resistant hypertensive patients.

To investigate the effects of salt loading on cardiopulmonary and arterial baroreceptor reflexes, 34 hypertensive patients underwent two 4-day periods with different dietary sodium intakes (70 and 370 meq/day). The patients were classified as salt-sensitive or salt-resistant depending on whether the mean arterial pressure value obtained on day 4 of high salt intake did or did not increase by 8% or more. In 22 patients cardiopulmonary and carotid baroreceptor reflexes were assessed during each dietary period by measuring the reflex responses to the application of -10 mm Hg lower body negative pressure and of +60 mm Hg increase in neck tissue pressure. Salt-resistant patients (n = 16) retained less sodium than salt-sensitive patients (n = 6) and showed a reduction in plasma norepinephrine and forearm vascular resistance during high sodium intake, whereas the salt-sensitive patients did not. During low sodium diet, no significant differences could be detected in the reflex responses to cardiopulmonary and carotid baroreceptor unloading between the two groups. High salt diet, however, potentiated the gain of cardiopulmonary baroreceptor reflex, which was expressed as the increase in plasma norepinephrine or forearm vascular resistance per millimeter of mercury decrease in pulmonary capillary wedge pressure, only in the salt-resistant hypertensive patients. In addition, the atrial natriuretic factor response to changes in pulmonary capillary wedge pressure was significantly enhanced by high salt intake only in the salt-resistant hypertensive patients. The reflex responses to carotid baroreceptor unloading were unaffected by salt loading in either group. In the remaining 12 patients, the hemodynamic effects of graded lower body negative pressure (-5, -10, -15 mm Hg) and neck tissue positive pressure (+30, +45, +60 mm Hg) were tested for both diets. Again, high salt intake significantly potentiated the cardiopulmonary baroreceptor reflex gain, expressed as the slope of the linear correlation between the changes in forearm vascular resistance (mm Hg/ml/min/100 g) and pulmonary capillary wedge pressure (mm Hg), in salt-resistant (from 3.8 +/- 0.9 to 7.2 +/- 1.0, p less than 0.05) but not in salt-sensitive patients (from 4.2 +/- 0.9 to 3.2 +/- 0.6, NS). In conclusion, the present study demonstrates that high salt diet potentiates cardiopulmonary baroreceptor reflexes and enhances atrial natriuretic factor response in salt-resistant but not in salt-sensitive hypertensive patients. The salt-induced plasticity of cardiopulmonary baroreceptor reflexes may exert a protective effect against the development of salt-induced hypertension by augmenting the reflex vasodilatory response to volume expansion.(ABSTRACT TRUNCATED AT 400 WORDS)

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↗

PubMed1989

Limited compensation by table salt for reduced salt within a meal.

Sixteen subjects, all of whom had said in a preliminary questionnaire that they normally added table salt to foods, were fed standard meals in the laboratory over 10 days. The meals were identical, except that on 5 days the meal had no added salt (containing 0.46 g sodium chloride) or had salt added to a level of 5.09 g. They were allowed free access to salt pots with the meals and used an average of 1.40 g table salt with the unsalted meal and 0.36 g with the salted meal, thus compensating for 22% of the difference in salt content of the meal. There was no difference in water consumption between the two types of meal. Nutrient intake from the rest of the diet did not differ between periods with high and low salt meals. The failure to compensate more fully for reduced salt in the foods can be attributed to the greater availability of table salt for perception; less table salt than salt incorporated in the foods is therefore required. Reduction of salt concentrations in purchased foods would be unlikely to be fully replaced by the consumer adding table salt.

Analysis of Variance↗

PubMed1988

Blood pressure, salt appetite and mortality of genetically hypertensive and normotensive rats maintained on high and low salt diets from weaning.

1. Blood pressure, bodyweight, saline preference and mortality rate were examined in spontaneously hypertensive rats (SHR) of the Okamoto strain and normotensive control Wistar-Kyoto (WKY) rats maintained on low (0.1% NaCl w/w), control (0.8% w/w) and high (3% w/w) salt diets from weaning until 6 months of age. 2. The growth rate of SHR on high salt diet was not significantly different from that on control diet but SHR maintained on a low salt diet exhibited a markedly reduced growth rate. While the growth rate of WKY on low salt diet was not significantly different from that on control diet, the bodyweights of WKY on high salt diet were significantly greater than those of animals on control diet. 3. While low salt diet markedly attenuated the development of hypertension in the SHR, high salt diet significantly exacerbated the blood pressure of this strain. Neither high nor low salt diet altered the blood pressure of WKY. 4. SHR on high and low salt diets had an increased mortality rate compared with SHR on control salt diet but these differences were of slight statistical significance. Conversely, WKY on all three diets exhibited similar mortalities over the 6-month observation period. There were no significant differences in mortalities between SHR and WKY on any diet. 5. The preference for 0.9% saline, when offered as a choice with water, was not significantly different between SHR on the different diets. WKY on high salt diet, however, exhibited a significantly reduced preference for saline over the 10-day test period compared with animals on control or low salt diet. 6. Thus dietary salt modulates the hypertension of SHR but not the blood pressure of WKY. SHR would appear to require more dietary sodium for normal growth and perhaps full expression of its hypertension. The higher and lower blood pressures of the SHR on high and low salt diet, respectively, were associated with increased mortality, which was a trend not seen in the WKY.

Animals↗

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↗

PubMed1986

High salt diet sensitizes cardiopulmonary baroreflexes in Dahl salt-resistant rats.

Compared with Dahl salt-resistant (R) rats, Dahl salt-sensitive (S) rats on a low salt diet have impaired cardiopulmonary baroreflex control of sympathetic nerve activity. The purpose of this study was to examine the sensitivity of cardiopulmonary baroreflex function in both strains of Dahl rats when they are challenged with a high salt diet. We studied Dahl R and S rats after 6 weeks of low and high salt diets. To assess cardiopulmonary baroreflex function, we measured decreases in splanchnic sympathetic nerve activity produced by increases in left ventricular end-diastolic pressure during graded volume expansion (dextran 75) after bilateral sinoaortic denervation. A given amount of infused volume produced comparable increases in left ventricular end-diastolic pressure in Dahl R rats on low and high salt diets but significantly greater decreases in sympathetic nerve activity in the high salt group than in the low salt group. Thus, the high salt diet augmented the sympathoinhibitory response to volume expansion in the Dahl R rats. In contrast, among the Dahl S rats equivalent increases in left ventricular end-diastolic pressure during volume expansion produced smaller sympathoinhibitory responses in the high salt group than in the low salt group. The gain of the cardiopulmonary baroreflex, expressed as the percentage decrease in sympathetic nerve activity per mm Hg increase in left ventricular end-diastolic pressure, was significantly increased by a high salt diet in Dahl R rats but tended to be decreased by a high salt diet in Dahl S rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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↗