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

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. Nonosmotic vasopressin release has been implicated in the water retention of these edematous disorders. The nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems in both experimental animals and in edematous patients. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin and activation of the renin-angiotensin system. These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. Neither total extracellular fluid volume nor blood volume is a determinant of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by a decrease in effective arterial blood volume (EABV) due to either a fall in cardiac output or peripheral arterial vasodilation. The acute response to a decrease in EABV involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The resultant renal vasoconstriction limits the distal tubular delivery of sodium and water, thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
Hypertension 1991 Nov
PMID:Unifying hypothesis of sodium and water regulation in health and disease. 193 81

The effects of dietary sodium restriction on the maintenance of blood pressure (BP) by sympathetic tone were evaluated in young versus more mature spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Sympathetic activity was assessed by BP responses to alpha 1-receptor blockade (prazosin), central inhibition of sympathetic outflow (clonidine), and by ganglionic blockade (hexamethonium). On regular sodium intake, SHR showed elevated BP and increased BP responses to sympathetic blockade at both 10 and 16 weeks of age. Sodium restriction to 9 or 17 mumols Na+/g food prevented or blunted development of hypertension in SHR when started at 4 weeks of age but did not affect BP when started at 10 weeks of age. Sodium restriction initiated in young SHR also prevented development of increased BP responses to sympathetic blockade. However, sodium restriction in more mature SHR did not decrease the increased BP responses to sympathetic blockade. We conclude that prevention of development of sympathetic hyperactivity in young SHR represents a major mechanism in the antihypertensive effect of sodium restriction in young SHR.
 ...
PMID:Dietary sodium restriction and blood pressure response to sympathetic blockade in young versus adolescent spontaneously hypertensive rats. 197 Feb 73

Epidemiological evidence suggests that low potassium intake is associated with the probability of occurrence of hypertension and stroke. The short-term response to increased potassium intake is increased sodium excretion as well as increased potassium excretion; the short-term response to increased sodium intake is increased potassium excretion as well as increased sodium excretion. In some experimental studies, increased amounts of potassium have been able to block the noxious influences of sodium. Sodium and potassium must be concomitantly considered in the investigation of the association of either of these cations with hypertension and cardiovascular disease. The chloride ion is also important for sodium's effects; its importance in potassium's effects has not been extensively explored.
Hypertension 1991 Jan
PMID:Sodium-potassium interaction in hypertension and hypertensive cardiovascular disease. 198 94

Nutritional-nonpharmacological approaches for the treatment and prevention of hypertension are of great interest. Sodium reduction is one of the primary methods recommended for these purposes. The general public is interested in the reduction of dietary sodium intake and has responded with a decrease in table salt use, the purchase of lowered sodium food products, and the use of food labels to help guide food purchases. Countervailing trends in the use of convenience foods and dining out increase the difficulty for individuals to lower sodium intake. Clinical trials that have used sodium reduction alone or in combination with other lifestyle therapies have demonstrated the feasibility of reducing dietary sodium intake from 30% to 50% for up to 4 years, in a variety of populations. Trials that used lifestyle and weight loss interventions have also achieved significant reductions in body weight and alcohol consumption and increases in physical activity. A variety of studies indicate that long-term sodium reduction is feasible and that it is acceptable to patients. No negative consequences of these interventions have been observed, and in some cases improvement in the intake of other nutrients has occurred. Nonpharmacological interventions have resulted in hypertension control in significant proportions of the trial populations. These studies demonstrate that the foregoing types of interventions can significantly contribute to hypertension treatment and prevention.
Hypertension 1991 Jan
PMID:Dietary sodium reduction for hypertension prevention and treatment. 198 1

The effects of dietary sodium on blood pressure in normotensive adults is not well characterized. The Study of Sodium and Blood Pressure (SNaP) is a randomized, double-blind crossover trial using a placebo or 96 meq sodium in 4-week treatment periods separated by a 2-week washout period. Before capsule treatment periods, participants were instructed in a low sodium diet for 10 weeks to reduce urinary sodium excretion to less than 35 meq/8 hr. The low sodium diet was continued throughout the capsule treatment periods. Participants (n = 48; 47 white, 1 black) were 79% male and had an average age of 52 years, a body mass index of 27.6, and a baseline blood pressure of 131/84 mm Hg. Baseline overnight urinary sodium excretion was 51 meq/8 hr and 19 meq/8 hr after the low sodium diet run-in period, before the capsule treatment periods began. Resting, seated blood pressure was measured twice at each visit in a standard fashion. Differences between sodium and placebo treatment periods were as follows: systolic blood pressure, 123.9 versus 120.3 mm Hg, respectively (p less than 0.001); diastolic blood pressure, 78.7 versus 76.4 mm Hg, respectively (p = 0.005); and sodium excretion, 51.3 versus 30.9 meq/8 hr, respectively (p less than 0.001). Both systolic and diastolic blood pressures increased significant amounts in normotensive adults on a low sodium diet supplemented with 96 meq/day sodium. Long-term effects and dose-response relations need further study.
Hypertension 1991 Jan
PMID:Sodium chloride raises blood pressure in normotensive subjects. The study of sodium and blood pressure. 198 6

We studied total exchangeable sodium, ion transport activity at maximal rate, and erythrocyte Na+ content in response to angiotensin converting enzyme inhibition in mild-to-moderate essential hypertensive patients with normal renal function. Twenty-five patients (mean age 56 years, range 40-62 years) who had abnormal red blood cell Na(+)-K(+)-Cl- cotransport or red blood cell Li(+)-Na+ countertransport were treated with either enalapril (20 mg daily) or hydrochlorothiazide (50 mg daily) during a 30-day period. During the period of enalapril treatment, Na(+)-K+ pump and Na(+)-K(+)-Cl- cotransport increased significantly from 4,282 +/- 255 to 5,236 +/- 325 mumol/l red blood cell/hr (p less than 0.01) and 166 +/- 21 to 220 +/- 24 mumol/l red blood cell/hr (p less than 0.05), respectively. Mean intracellular Na+ content in erythrocytes decreased from 11.4 +/- 0.40 to 10.0 +/- 0.33 mmol/l (p less than 0.01) and exchangeable Na+ from 39.8 +/- 0.6 mmol/kg to 35.6 +/- 0.6 mmol/kg (p less than 0.001). Sodium reduction correlated with the recovery of Na(+)-K(+)-Cl- cotransport activity (r = -0.65, p less than 0.01). During treatment, systolic and diastolic blood pressures were reduced significantly (p less than 0.01). In 12 patients treated with hydrochlorothiazide, Na(+)-K(+)-Cl- cotransport, Na(+)-K+ pump, Na(+)-Li+ countertransport, and Na+ permeability did not change significantly while Na+ content decreased from 11.7 +/- 0.3 to 10.3 +/- 0.2 mmol/l (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Mar
PMID:Recovery of erythrocyte Na(+)-K(+)-Cl- cotransport activity by enalapril. 199 65

The relations of sodium, potassium, calcium, and magnesium to blood pressure were investigated in four groups of men (119 high-mountain Yi farmers, 114 mountainside Yi farmers, 89 Yi migrants, and 97 Han people) with a wide range of electrolyte intake in Puge County, Sichuan Province, People's Republic of China. Electrolytes were measured in diet, serum, and urine. Sodium excretion was 73.9 mmol/24 hr in high-mountain Yi farmers, 117.9 mmol/24 hr in mountainside Yi farmers, 159.4 mmol/24 hr in Yi migrants, and 186.0 mmol/24 hr in the Han people. In ecological correlation analysis, dietary and urinary sodium were significantly and positively correlated with both systolic and diastolic pressure, whereas serum sodium showed no relation with blood pressure. In diet, serum, and urine, potassium was negatively related to systolic and diastolic pressure, whereas the sodium/potassium ratio showed a positive association. With regard to calcium, only urinary excretion was significantly and positively related to blood pressure. No relation was found between magnesium and blood pressure. Analyses at the individual level confirmed the results for sodium and potassium seen at the ecological level, but in addition, dietary calcium and magnesium were significantly and negatively correlated to both systolic and diastolic pressure, and urinary magnesium was inversely related to diastolic pressure. These relations persisted after controlling for age, body mass index (kg/m2), heart rate, alcohol, and total energy intake in multiple regression analysis performed separately for electrolytes in diet, serum, and urine. In multiple regression analysis, an increase in sodium intake of 100 mmol/day corresponded to an increase of 2.3 mm Hg systolic blood pressure and 1/8 mm Hg diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Mar
PMID:Relation of electrolytes to blood pressure in men. The Yi people study. 199 67

Sodium may contribute to the pathogenesis of hypertension by impairing arterial baroreceptor reflex function. The objectives of this study were to 1) determine whether a high sodium diet depresses arterial baroreceptor reflex function in normotensive humans, and 2) determine whether alterations in baroreceptor reflex function are related to changes in arterial compliance. Seventeen normotensive men, aged 30 +/- 2 years, received 10 and 200 meq sodium per day diets, each for 5 days, in a randomized crossover trial. Carotid baroreceptor reflex function was assessed by measuring the blood pressure response to sequential neck suction (0, -10, -20, and -30 mm Hg) and neck pressure (0, +10, +20, and +30 mm Hg). Forearm vascular resistance was determined by venous occlusion plethysmography. Arterial compliance was evaluated by calculating the quotient of the diastolic blood pressure decay time constant and forearm vascular resistance. Blood pressure averaged 124 +/- 3/62 +/- 2 mm Hg on the low sodium diet and 122 +/- 3/60 +/- 2 mm Hg on the high sodium diet (p = NS). Baroreceptor reflex slopes representing the systolic and diastolic blood pressure responses to changes in neck chamber pressure were steeper in the subjects when randomly assigned to low sodium diet than to high sodium diet. Diastolic blood pressure decay time and forearm arterial compliance were similar during low and high sodium intake. We conclude that short-term exposure to a high sodium diet depresses carotid baroreceptor reflex function in normotensive humans. This observation cannot be attributed to changes in the arterial compliance.
Hypertension 1991 Jun
PMID:Sodium depresses arterial baroreceptor reflex function in normotensive humans. 204 81

In each of two experiments, adult, male Sprague-Dawley rats were deprived of copper and were subjected to the chronic stress of close confinement. A 2 X 2 factorial design was used because both copper deficiency and stress have been implicated in the regulation of blood pressure and are implicated in a major consequence of human hypertension--ischemic heart disease. Copper deficiency was verified by a decrease in copper in several organs. Both copper deficiency and stress increased blood pressure; results were independent. Sodium in heart was increased by deficiency in both experiments, but was increased in brain in only the second experiment. The combination of stress and deficiency produced an increase in mortality in one of two experiments. A decrease in cholesterol in plasma due to stress is consistent with earlier data from rats but is in contrast to data from humans. Both stress and copper deficiency produce potentially adverse changes in cardiovascular physiology and the chemistry of brain, heart and other organs. These results may be germane to humans because stress is frequent and some diets are low in copper.
 ...
PMID:The effects of dietary copper deficiency and psychological stress on blood pressure in rats. 206 2

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
 ...
PMID:Metabolic considerations in hypertension. 207 23


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>