Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the possible involvement of ANP in the salt dependent hypertension of the DS rats the concentrations of immunoreactive atrial natriuretic peptides (ANP-IR) in atria, plasma and brain of salt loaded and control fed DS and DR rats were determined. On a low salt diet the ANP-IR concentrations in atria, hypothalamus and basal ganglia of DS rats were higher versus DR rats. Salt loading results in a decrease of ANP-IR in left DS atria and an increase in plasma and brain stem of DS rat versus control and DR rat. The data are compared with other studies about ANP performed in Dahl rats, SHR and WKY rats. The possible reasons for the found distribution of ANP-IR are discussed.
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PMID:ANP concentrations of atria, plasma and brain in Dahl S (DS) and Dahl R (DR) rats. 214 Jul 37

In order to investigate the effects of atrial natriuretic polypeptides (ANP) on hypertensive glomerular lesions, ANP was administered intravenously by osmotic minipumps to 20 15-week-old male spontaneously hypertensive rats (SHRs) in a sustained hypertensive stage. ANP was infused at the rate of 100 ng/hour/rat (the ANP group). Saline was similarly administered to 19 age-matched SHRs (the control group). The rats were sacrificed on the seventh day. Semiquantitative evaluation of the renal tissue revealed no significant difference in glomerular sclerosis between the 2 groups. However, segmental hyalinosis in glomeruli was more accentuated in the ANP group than in the control group. As it is suggested that hyalinosis in glomeruli is related to the elevated intracapillary pressure, the results of the present work were in accordance with reports that ANP increases glomerular capillary pressure by preglomerular vasodilation and postglomerular vasoconstriction. It should be determined whether endogenous ANP works as an aggravating factor for glomerular injuries in the natural course of hypertension.
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PMID:Effects of chronic administration of atrial natriuretic polypeptide on glomerular lesions in spontaneously hypertensive rats. 214 67

The aim of the present study was to determine if elevations in salt intake were coupled to increases in renal alpha 2-adrenergic receptors in SHR that differ in their blood pressure response to high salt diets. Salt-resistant spontaneously hypertensive rats (SHR-R), which do not increase their blood pressure in response to high salt intake, and salt-sensitive spontaneously hypertensive rats (SHR-S), which do exhibit significant elevations in blood pressure on high salt diets (3.15% NaCl), were used. Radioligand binding studies using [3H]rauwolscine were performed on 6- and 11-week-old SHR-S and Wistar-Kyoto (WKY) rats to determine the effects of age, strain, and salt intake on alpha 2-adrenergic receptor number and affinity. One week of high salt intake significantly increased blood pressure 22% in 6-week-old SHR-S and increased the blood pressure of 11-week-old SHR-S 12% without altering WKY rat controls. This treatment did not significantly increase renal alpha 2-adrenergic receptors in either SHR-S or WKY rats. SHR-S had significantly higher numbers of renal alpha 2-adrenergic receptors than WKY rats on the high salt diets. One week of high (3.15%) or low (0.05%) salt intake did not significantly alter renal alpha 2-adrenergic receptor number in 11-week-old SHR-S or WKY rats; however, blood pressure was significantly elevated in the SHR-S (175.0 +/- 3.5 versus 196.0 +/- 3.0 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Jul
PMID:Upregulation of renal alpha 2-adrenergic receptors is not indicative of salt-related increases in blood pressure in spontaneously hypertensive rats. 216 82

Sodium chloride has no clearly established local direct action on blood vessels to produce constriction; on the contrary, it has an immediate local indirect action via osmolality, which produces vasodilation. Thus in order to explain salt-induced hypertension, a delayed remote indirect vasoconstrictor action must be postulated. This indirect vasoconstrictor action is apparently the result of volume expansion. Acute volume expansion imparts three physiologic properties to the plasma; these are the ability to inhibit Na,K-ATPase and the Na-K pump, to cause natriuresis, and to sensitize blood vessels to vasoconstrictor agents. Similarly, low-renin, volume-expanded hypertension endows the plasma with the capacity to inhibit the Na,K-ATPase pump, to sensitize blood vessels to vasoconstrictor agents, and to raise blood pressure. These properties apparently result from a circulating digitalislike substance(s), perhaps derived from the hypothalamus and/or adrenals. We here review the considerable effort expended in identifying the agent or agents, and conclude that both steroidal and peptidic structure must be considered. Regardless of its structure, we hypothesize that when sodium excretion does not keep pace with sodium intake, its release leads to increased contractile activity of cardiac and vascular smooth muscle and hence hypertension. Inhibition of the Na-K pump increases the intracellular sodium concentration, particularly when superimposed on genetic- or aldosterone-induced increased sodium permeability, resulting in depolarization and increased calcium influx (vascular smooth muscle) or altered Na(+)-Ca2+ exchange and decreased calcium efflux (heart muscle). The increased intracellular calcium concentration then accounts for the increased contractile activity. Depolarization may also increase the sensitivity of vascular smooth muscle to vasoconstrictor agents such as norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Digitalislike circulating factor in hypertension: potential messenger between salt balance and intracellular sodium. 217 7

Spontaneously hypertensive rats (SHR) were uninephrectomized (UNX) at 6 wk of age and given either standard chow (CON), low-sodium chow (LSC), or standard chow and hydrochlorothiazide (HCTZ) added to the drinking water. Severe hypertension developed in all three groups. Forty-two weeks after UNX, proteinuria and glomerular sclerosis were significantly lower in LSC than in CON or HCTZ. The protective effect of salt restriction did not depend upon alterations in plasma renin concentration or glomerular hemodynamics. Micropuncture revealed that glomerular pressure was high in all three groups. Renal hypertrophy assessed by kidney weight, kidney-to-body weight ratio, glomerular volume, and glomerular capillary radius were reduced by salt restriction. These findings suggest that, in the setting of glomerular hypertension, hypertrophy promotes sclerosis. Salt restriction inhibits compensatory kidney growth and protects the kidney.
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PMID:Superiority of salt restriction over diuretics in reducing renal hypertrophy and injury in uninephrectomized SHR. 219 43

Body weight reduction in the overweight hypertensive patient was found to reduce blood pressure, irrespective of the daily urinary sodium excretion. Significant blood pressure reductions were achieved while the urine sodium excretion was between 165-185 mEq/day. Salt restriction resulting in a significant decrease of the 24-hour urine sodium from 192-110 mEq/24-hours did not change the blood pressure. Some of the studies indicating a reduction in blood pressure, did not take into account the changes in body weight, while on sodium restriction. Thus sodium restriction in the treatment of hypertension has not been uniformly found to reduce the blood pressure. Although there is much evidence in favour of the involvement of sodium in the regulation of blood pressure, there is no convincing evidence that dietary sodium restriction can be of use as a therapeutic modality in the treatment of hypertension in the overweight hypertensive patient.
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PMID:Energy restriction or salt restriction in the treatment of overweight hypertension. Which one? A point of view. 220 51

Metabolic acidosis has recently been observed in rat models of salt-sensitive genetic hypertension. To test the hypothesis that salt sensitivity in humans may be associated with abnormal acid-base homeostasis, we performed arterial blood gas analyses in young (20-31 years old) normotensive subjects (n = 40) who were placed on a low salt diet (20 mmol NaCl/day) for 2 weeks with either 200 mmol sodium chloride or placebo added to the low salt diet for 1 week each in a randomized, single-blind crossover order. Furthermore, a subset of the subjects (seven salt-sensitive and eight salt-resistant) received 200 mmol sodium/day as the citrate salt as a supplement to the low salt diet for a third week. During each regimen, blood pressure as well as arterial pH and bicarbonate levels were measured. Salt sensitivity was defined as a significant drop in mean arterial pressure greater than 3 mm Hg (mean of 30 readings taken during each diet, p less than 0.05) while the subject was on the low salt diet. According to this definition, 16 subjects were salt-sensitive and 24 salt-resistant. During the high sodium chloride regimen, arterial pH and bicarbonate levels were significantly lower in the salt-sensitive than in the salt-resistant group (p less than 0.0001). The increase in blood pressure caused by sodium chloride correlated inversely to the arterial pH (r = -0.57, p = 0.0002) and bicarbonate levels (r = -0.52, p = 0.0007) during the high salt diet. Sodium chloride increased mean arterial blood pressure in the salt-sensitive subjects; sodium citrate did not. Sodium citrate led to an increase in pH and bicarbonate levels in both groups. Our finding that a sodium chloride-induced rise in blood pressure is associated with lower arterial plasma pH and bicarbonate levels points to an abnormality in renal acid-base regulation in salt-sensitive subjects.
Hypertension 1990 Oct
PMID:Salt sensitivity in humans is associated with abnormal acid-base regulation. 221 Aug 8

The dependence of blood pressure on nutritional factors is reviewed in the light of possible therapeutic consequences. Salt restriction, increased administration of potassium, restriction of alcohol intake, weight loss and prescription of fish-oil are discussed by review of own and published data. All these measures may contribute to a reduction of hypertension although to a variable extent. They should be envisaged as therapeutic alternatives to drugs in mild hypertension.
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PMID:[Nutrition and hypertension: what are the goals?]. 221 33

The reduction in blood pressure to normotensive levels within 3 hours of unclipping the one-kidney, one clip Goldblatt hypertensive rat has been attributed to the release of potent blood pressure-lowering lipids, one of which is thought to be identical to platelet activating factor. The specific platelet activating factor receptor antagonist WEB 2086 was infused intravenously into hypertensive one-kidney, one clip rats, and the mean arterial blood pressure changes after unclipping were examined. Before infusion, blocking doses of WEB 2086 were confirmed to effectively abolish the fall in blood pressure induced by exogenous platelet activating factor. Serotonin release in response to exogenous platelet activating factor was also inhibited in platelets preincubated with plasma from rats infused with the antagonist. Hypertensive rats were given a bolus blocking dose of WEB 2086 (5 mg/kg i.v.) and the same dose by infusion (5 mg/kg/hr i.v.) before they were unclipped. A control group was given a bolus volume of saline and infused with saline before unclipping. In WEB 2086-treated rats, blood pressure fell from a baseline mean of 181 +/- 13.0 to 125 +/- 23 mm Hg after 4 hours, a fall of 28%. Saline-treated rats fell from a mean of 194 +/- 23 to 127 +/- 25 mm Hg (33%). There was no significant difference in the blood pressure fall between the two groups. Therefore, platelet activating factor is unlikely to be responsible for the restoration of normal blood pressure after unclipping the Goldblatt hypertensive rat. We attribute the fall in blood pressure to other presently unidentified renomedullary lipids.
Hypertension 1990 Jun
PMID:Platelet activating factor and one-kidney, one clip hypertension. 234 25

The role of calcitonin gene-related peptide (CGRP)-containing vasodilator nerves in maintenance of hypertension was investigated in the perfused mesenteric vascular beds isolated from spontaneously hypertensive rats (SHR), deoxycorticosterone-salt-induced hypertensive rats (DOCA-Salt-HR) and corresponding normotensive control rats (Wistar Kyoto rats, WKY and Wistar rats, NR). In the mesenteric artery with an active tone, the neurogenic vasodilation induced by perivascular nerve stimulation (PNS, 0.5-8 Hz), which was mediated by CGRP nerves, was markedly decreased in adult SHR (15-week-old) when compared with age-matched WKY, whereas the vasodilation in DOCA-Salt-HR was similar in magnitude to that in NR. The vasodilator response to exogenously applied CGRP was greater in SHR than in WKY, whereas no difference was found between DOCA-Salt-HR and NR. The neurogenic release of CGRP-like immunoreactivity (CGRP-LI) induced by PNS of the mesenteric artery was significantly decreased in SHR compared to that of WKY. In addition, immunohistochemical studies showed decreased populations of CGRP-LI fibers in the mesenteric artery of SHR compared to those in WKY. These results suggest that CGRP-containing vasodilator innervation is greatly decreased in SHR with established hypertension. It is also suggested that the decreased vasodilator mechanism by CGRP-containing nerves contributes to the maintenance of hypertension.
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PMID:Changes in calcitonin gene-related peptide (CGRP)-containing vasodilator nerve activity in hypertension. 239 Jul 22


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