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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. To determine the effect of chloride ion on the development of hypertension and the incidence of cerebral lesions in stroke-prone spontaneously hypertensive rats (SHRSP), groups of 10 rats were administered chronically with either 171 mmol/L sodium chloride or equimolar sodium provided as sodium citrate in the drinking water from the age of 12 weeks. 2. The life span was significantly extended in SHRSP given sodium citrate (336 +/- 28 vs 246 +/- 26 days, mean +/- s.e.m., P less than 0.05) but their development of hypertension was not different from SHRSP given sodium chloride. 3. In order to determine the role of calcium homeostasis, calcium in urine was collected. Urinary calcium in SHRSP given sodium citrate was significantly decreased (1.0 +/- 0.12 vs 1.8 +/- 0.18 mg/24 h urine, P less than 0.05). 4. If the normal life span is 320 +/- 35 days, this suggests that chloride ion ingested with sodium accelerates the development of cerebrovascular diseases, and that increased urinary calcium excretion may be related to this adverse chloride effect on the development of hypertension in SHRSP.
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PMID:Chloride ion ingested with sodium affects the development of cerebral lesions in stroke-prone spontaneously hypertensive rats. 191 41

The mineral elements sodium, potassium, calcium and magnesium play a central role in the normal regulation of blood pressure. In particular, these mineral elements have important interrelationships in the control of arterial resistance. These elements, especially sodium and potassium, also regulate the fluid balance of the body and, hence, influence the cardiac output. Evidence shows that the present levels of intake of mineral elements are not optimum for maintaining normal blood pressure but predispose to the development of arterial hypertension. Research results suggest that without sodium chloride (common salt) and other sodium compounds being added to the diet arterial hypertension would be virtually non existent. Moreover, blood pressure would not rise with age. In communities with a high consumption of added sodium, a high intake of potassium and, possibly, magnesium seem to protect against the development of arterial hypertension and the rise of blood pressure with age. A marked reduction of sodium intake is effective in treating even severe hypertension. A moderate restriction of sodium intake or an increase in potassium intake exert remarkable antihypertensive effects, at least in some hypertensive patients. Magnesium and possibly also calcium supplements may be effective in reducing blood pressure in some hypertensives. In hypertensive patients treated with drugs sodium restriction and potassium and magnesium supplementation enhance the therapeutic effect, reduce the number and dosage, and lessen the adverse effects of prescribed antihypertensive drugs. Hence, a fall in sodium consumption and increases in potassium and magnesium consumption are useful in preventing and treating arterial hypertension.
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PMID:Minerals and blood pressure. 193 Sep 21

Post-renal transplant hypertension remains a common problem. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. Before the development of cyclosporine, renin-dependent hypertension was the dominant pathophysiological mechanism but now, with the widespread use of cyclosporine, a salt-dependent mechanism is the major one. In severe "inappropriate" hypertension, potentially surgically remediable causes such as renal artery stenosis of the allograft artery or renin release from the native kidneys should be considered. Cyclosporine causes hypertension in normal subjects and in all solid organ transplants. The most likely mechanism is renal vasoconstriction with subtle retention of sodium chloride together with systemic vasoconstriction. The vasoconstriction, as yet, is not associated with any specific vasoconstricting agent nor does there appear to be a specific antagonist. Indeed, increased sensitivity to many different vasoconstrictors has been demonstrated. The major site of vasoconstriction appears to be in the afferent arteriole, and optimum antihypertensive therapy is probably provided by calcium channel blockers if the hypertension is due to cyclosporine. Because post-renal transplant hypertension is often multifactorial in origin, however, it is not surprising that the use of combined antihypertensives is often necessary.
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PMID:Pathophysiology and treatment of posttransplant hypertension. 193 42

The present study investigated the effect of the anion accompanying sodium on the development of angiotensin II-induced hypertension in rats and the role of the sympathetic nervous system and extracellular fluid volume in its mechanism. Hypertension was induced by intraperitoneal infusion of angiotensin II (125 ng/min) for 12 days via miniosmotic pump. High dietary intake of sodium chloride significantly augmented the angiotensin II-induced hypertension (mean blood pressure on day 13, 165 +/- 6 versus 142 +/- 6 mm Hg, p less than 0.05), but equimolar sodium loading provided as sodium citrate failed to enhance angiotensin II hypertension (140 +/- 6 mm Hg). Plasma norepinephrine concentration in the conscious, resting state increased with sodium chloride loading in angiotensin II-infused rats (594 +/- 42 versus 312 +/- 37 pg/ml, p less than 0.01), but it remained unchanged with sodium citrate loading (324 +/- 23 pg/ml). Correspondingly, maximum response to hexamethonium bromide, a ganglion blocker, was greater in sodium chloride-loaded angiotensin II rats (77.7 +/- 4.6 mm Hg) than that in angiotensin II (59.7 +/- 5.1 mm Hg) or in sodium citrate-loaded angiotensin II (57.7 +/- 4.2 mm Hg) rats. Moreover, extracellular fluid volume, measured as Na2(35)SO4 space, increased in sodium chloride-loaded angiotensin II rats (427 +/- 18 ml/kg body wt) as compared with that in angiotensin II rats (375 +/- 15 ml/kg body wt) but not when compared with volume in sodium citrate-loaded angiotensin II (389 +/- 7 ml/kg body wt) rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Nov
PMID:Role of chloride in angiotensin II-induced salt-sensitive hypertension. 193 65

This review first summarizes evidence from animals and humans for and against a role for dietary sodium in the genesis and treatment of hypertension. The evidence for its role is strongest in those subjects with impaired ability to excrete sodium because of organic renal disease or mineralocorticoid excess. Here, restriction of dietary sodium promptly lowers pressure. Its role in the genesis of essential hypertension is more controversial. Nevertheless, it appears that some patients with mild to moderate essential hypertension respond to moderate sodium restriction with a modest fall in pressure. This restriction also seems to reduce the amount of antihypertensive medication needed to keep pressure under control. Next, the mechanism of the pressure response to dietary sodium chloride is considered, with emphasis on potassium depletion and increased plasma levels of prohypertensive sodium pump inhibitor and antihypertensive atrial natriuretic peptide. The evidence for a primary role for dietary potassium in the genesis of hypertension then is summarized; certain subsets of subjects with a high incidence of hypertension also have a lower potassium intake. Some investigators have found that dietary potassium supplementation lowers pressure in established hypertension. This may result from natriuresis and from vasodilation subsequent to stimulation of Na+,K(+)-ATPase in vascular smooth muscle and adrenergic nerve terminals. After the role of dietary calcium is discussed, practical aspects of dietary sodium restriction and dietary potassium supplementation in the therapy for established hypertension are considered. The review concludes with comments on their possible roles in the prevention of hypertension.
Hypertension 1991 Nov
PMID:Roles of sodium, potassium, calcium, and natriuretic factors in hypertension. 193 82

Overall 78 men were examined. Of these, 30 presented with borderline arterial hypertension (BAH), 30 with stage I essential hypertension (EH), and 18 healthy subjects served as control. To assess osmoregulating and natriuretic renal functions, water and water plus salt were administered (at a rate of 22 ml water or isotonic sodium chloride per kg bw). Use was made of classic approaches in this case, with the determination of K+, Na+ excretion, blood plasma and urine osmolarity, calculation of the concentration index, clearance of osmotic-active substances and free water, total reabsorption of Na in the distal parts of nephron and intensity of that process. Besides, flame photometry was employed to measure blood K+, Na+ concentration and RIA to examine plasma renin activity. The data obtained indicate the heterogeneity of the patients with BAH and stage I EN according to the response to water and water and salt administration. Approximately 1/3 of the patients showed a tendency towards water retention in the body as well, which is common to patients with the volume-dependent form of arterial hypertension. In that case the compensatory potentialities of modulating renin-angiotensin system activity were preserved.
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PMID:[The osmoregulatory and natriuretic functions of the kidneys in the early stages of the evolution of hypertension]. 194 58

Intracerebroventricular (i.c.v.) infusion of hypertonic sodium chloride solution increased blood pressure (BP) and shortened heart period (interbeat-interval: IBI) that is why an impairment in baroreflex regulation is believed to be part of that process. Therefore, in anaesthetized rats (1.35 g urethane/kg BW) the baroreceptor-heart reflex (BHR) was tested before and during i.c.v. infusion (15 min) of isotonic or hypertonic (0.6 M, 1.0 M) sodium chloride solution by inducing an acute BP rise by i.v. pressoric agents (phenylephrine, methoxamine). The evoked reflex prolongation of the IBI was taken to estimate the sensitivity of that BHR (delta ms/mm Hg). Whilst i.c.v. infusion of isotonic sodium chloride solution did not affect BHR sensitivity, hypertonic sodium chloride solution not only elevated BP and shortened IBI but also reset and impaired the BHR. Therefore, an increased central sensitivity to sodium chloride might not only increase BP but also impair the buffering capacity of the BHR against this rise and in this way support development of hypertension.
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PMID:Intracerebroventricular administration of hypertonic sodium chloride solution reduces the sensitivity of the baroreceptor heart reflex in anaesthetized rats. 195 93

The relation between dietary intake of sodium chloride and blood pressure levels remains controversial. The critical questions concern whether there is a susceptible subgroup at risk of elevated blood pressure because of sodium chloride consumption. If there is such a subgroup, what is its size and how can it be identified? Further clinical trials are needed to determine the long-term effects of sodium chloride reduction on blood pressure. The risk of disease, including stroke and coronary heart disease, is linear with blood pressure levels. A small change in blood pressure can have a relatively large impact on disease, even within the normal range of blood pressure.
Hypertension 1991 Jan
PMID:Research and policy directions. Salt and blood pressure. 198 7

The purpose of this study was to examine the effect of the sulfate ion on blood pressure in DOCA-salt hypertension, which involves increased sympathetic nervous activity. Male Wistar rats were divided into four groups, and received one of the following drinking solutions: distilled water [control], 171 mmol/L sodium chloride [NaCl group], 171 mmol/L sodium chloride plus 12 mmol/L magnesium sulfate [S(+) group], or 171 mmol/L sodium chloride plus 12 mmol/L magnesium chloride [S(-) group]. In the S(+) group, the elevation of systolic blood pressure (SBP; mm Hg) was significantly attenuated (168 +/- 17 v 213 +/- 26, P less than .005) and intraerythrocyte calcium concentration (R-Ca; mumol/L cells) was significantly lower (11.5 +/- 3.0 v 17.4 +/- 6.5, P less than .05) than in the S(-) group. The cardiac norepinephrine content (H-NE; ng/100 g tissue) of the S(+) group was significantly lower than that of the S(-) group. SBP was correlated negatively with H-NE (r = -0.70, P less than .001) and positively with R-Ca (r = 0.45, P less than .005). R-Ca was negatively correlated with H-NE (r = -0.36, P less than .05). These results suggest that the replacement of chloride with sulfate ion suppresses the development of hypertension in DOCA-salt rats at least in part by its inhibitory effect on sympathetic nervous activity through the decreased intracellular calcium concentration.
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PMID:Suppressive effect of sulfate on the development of hypertension in DOCA-salt hypertensive rats. 202 48

The Dahl salt-sensitive rat was used to investigate the effect of hypertension on indexes of copper status and to determine the extent to which dietary manipulation of copper attenuated, or exacerbated, the rate of sodium chloride-induced hypertension. Weanling salt-sensitive rats were fed, in a 2 x 3 factorial design, one of six diets that contained one of three levels of copper (2.0 micrograms/g marginal, 12 micrograms/g adequate, or 50 micrograms/g supplemental) and either control (0.4%) or high (4%) levels of sodium. Diets were fed to the rats for 11 weeks. Rats fed the high sodium diets were characterized by high plasma copper concentrations and ceruloplasmin activities compared with their respective control sodium rats. The magnitude of the sodium-induced rise in plasma copper and ceruloplasmin was affected by dietary copper intake; however, dietary copper intake had no effect on the development of hypertension in the high sodium groups. These results suggest that altered copper metabolism is secondary, rather than primary, to the development of sodium chloride-induced hypertension in the salt-sensitive rat. Red blood cell superoxide dismutase activity was reduced in rats fed the low copper diets compared with the adequate and supplemented copper groups. At the lower levels of copper intake, sodium chloride-induced hypertension increased red blood cell superoxide dismutase activity in a manner consistent with the plasma copper and ceruloplasmin changes observed. However, at adequate or supplemental levels of dietary copper, red blood cell superoxide dismutase activity plateaued, suggesting possible saturation of copper at sites of hematopoeisis.
Hypertension 1991 Jun
PMID:Influence of hypertension and dietary copper on indexes of copper status in rats. 204 41


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