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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute volume expansion increases the intrathoracic blood volume thus endowing the plasma with an increased capacity to cause a natriuresis, to inhibit Na-K-ATPase and stimulate vascular reactivity. It is not known whether these changes, which stem from a common stimulus are due to a change in the concentration of one substance or several. It is proposed that in essential hypertension a genetic abnormality of the kidney causes a difficulty in excreting sodium. This leads to an initial blood volume expansion which causes the observed rise in the plasma's capacity to inhibit sodium transport, and to the increased vascular tone. Eventually the increase in tone of the arterial smooth muscle causes the blood pressure to rise, while the increase in tone of the smooth muscle of the veins diminishes venous compliance thus causing a shift of blood from the periphery to the chest thus providing the stimulus for the persistent rise in the plasma's capacity to increase vascular reactivity, even though total blood volume may have returned to normal.
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PMID:The concept of the natriuretic hormone and its relation to hypertension. 389 7

The hemodynamic, hormonal, and renal responses to alterations in dietary potassium were studied in normotensive and hypertensive subjects. In a short-term study, nine normotensive and nine hypertensive young men received a normal diet and low potassium, high potassium, and high potassium/low sodium diets for 1 week, each. The long-term effect of potassium supplementation (normal diet plus 96 mmol KC1/d for 8 weeks) was evaluated in 17 patients with essential hypertension. Blood pressure did not change significantly during short-term alterations of potassium intake but decreased during long-term supplementation (from 152.2 +/- 3.5/99.6 +/- 1.9 mm Hg to 137.4 +/- 2.9/89.1 +/- 1.4 mm Hg). High dietary potassium induced a significant but transient natriuresis. Plasma potassium concentration was increased during long- but not during short-term high potassium intake. In contrast to plasma renin activity (PRA) and aldosterone, urinary kallikrein was consistently stimulated during long-term potassium supplementation. The plasma concentrations of adrenaline and noradrenaline were significantly higher in hypertensive than in normotensive subjects and were not markedly altered by the dietary changes. It is concluded that long- but not short-term potassium supplementation lowers blood pressure in patients with essential hypertension. The antihypertensive effect may be mediated by potassium-induced natriuresis, by a stimulation of Na-K-ATPase secondary to increased plasma potassium levels, and/or by a modulation of the renin-angiotensin-aldosterone, kallikrein-kinin, and sympathetic nervous systems.
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PMID:Hemodynamic, renal, and hormonal responses to changes in dietary potassium in normotensive and hypertensive man: long-term antihypertensive effect of potassium supplementation in essential hypertension. 392 52

In this study erythrocyte phosphate release depended on the intracellular hydrolysis of organic phosphate esters. Total phosphate release was increased in essential hypertension, which suggests an elevated phosphate ester metabolism. Ouabain-sensitive phosphate release was decreased, and the ratio of intracellular Na+/K+ concentrations was increased, a finding consistent with a diminished Na-K-ATPase activity. Furosemide in a concentration of 1.0 mmol/L inhibited erythrocyte phosphate release by half, probably owing to nonspecific membrane effects. The combination of ouabain and furosemide reduced phosphate transfer to a higher degree than did each substance individually. Because of the nonspecific alteration of erythrocyte membrane permeability by furosemide in a concentration of 1.0 mmol/L, ouabain-insensitive, furosemide-sensitive phosphate release and ouabain-insensitive, furosemide-sensitive Na+ efflux (Na-K cotransport) must not be regarded uncritically as specific transport systems.
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PMID:Erythrocyte phosphate release in essential hypertension. 399 26

The effect of salt and/or volume depletion has been tested in 6 end-stage renal disease and 11 essential hypertensive patients (HTA) on red blood cell (RBC) ionic fluxes. Volume depletion promotes an increase in the RBC Na-K ATPase activity with, as a result, a significant decrease in intracellular sodium concentration [Na)ic). Moreover, a factor has been found in the plasma of uremic subjects which causes natriuresis when injected in rat renal arteries. The concentration of this factor decreases during dialysis in relation to the weight loss and the increase in the RBC Na-K pump activity. In essential hypertension, the effect of a low salt diet on the blood pressure is correlated with the improvement of RBC Na-K ATPase activity. These experiments illustrate the presence of a Na-K ATPase inhibitor in the plasma of these subjects, dependent on sodium and water balance.
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PMID:Arguments for the presence of a Na-K ATPase pump inhibitor in the plasma of uremic and essential hypertensive patients. 401 65

Previous investigations have demonstrated an increased amount of a sodium pump inhibitor (N.H.) in plasma from humans with essential hypertension and from animals with various forms of experimental hypertension. The present study has employed Sephadex column and C18 reverse phase separation of urines from patients with essential hypertension and normal controls to distinguish "high", "intermediate" and "low" molecular weight forms of N.H., measured through properties of Na-K-ATPase inhibition and digoxin-like immunoreactivity. The major difference between hypertensive and normotensive urines was a highly significant increase in the "intermediate" molecular weight form of N.H., as measured by Na-K-ATPase inhibition. In contrast, digoxin-like immunoreactivity was significantly decreased in urine from hypertensive patients. The results are compatible with an hypothesis that the defect in some forms of essential hypertension may be partial inhibition of enzymatic conversion of intermediate to final form of N.H., with the increased sodium pump inhibition primarily related to the precursor.
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PMID:Observations on the "cascade" of Na-K-ATPase inhibitory and digoxin-like immunoreactive material in human urine: possible relevance to essential hypertension. 401 67

Bovine hypothalamus contains a stable, low molecular weight substance with ouabain-like properties. To further study its mechanism of action and potential physiological importance we examined its effects on purified Na+-K+-ATPase in a kinetic coupled-enzyme assay. Under optimal conditions up to 95% of Na+-K+-ATPase activity could be inhibited by the factor. Mg2+ is required for maximal inhibitory activity, but ligand requirements for optimal activity are otherwise distinct from those of both ouabain and vanadate. Inhibition is reversed by high concentrations of sodium chloride plus EDTA. Kinetic analysis yielded a Ki = 1.4 nM. The hypothalamic factor is a high-affinity reversible inhibitor of Na+-K+-ATPase, being at least as potent as the cardiac glycoside ouabain and may be a circulating inhibitor of sodium transport, which appears to be associated with experimental volume-expanded hypertension and human essential hypertension.
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PMID:Hypothalamic sodium-transport inhibitor is a high-affinity reversible inhibitor of Na+-K+-ATPase. 609 82

The presence of a circulating Na+ pump inhibitor has been assessed in 112 subjects by studying the effects of deproteinized plasma on ouabain binding to erythrocytes and/or inhibition of Na+-K+-ATPase activity. High levels of an inhibitor possessing some digitalis-like properties, were associated with essential hypertension, hypertensive heredity, treatment of hypertension with beta-blocking agents and high sodium intake. Low levels were found in hypertensives on diuretics, patients with chronic renal failure and normotensive controls. These observations are consistent with a possible role of this circulating inhibitor in the control of sodium balance and in hypertension.
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PMID:[Circulating inhibitor of the Na+-K+ pump in essential hypertension. Physiological and pharmacological variations]. 609 38

In order to study cation transport in vivo the changes in plasma and red cell rubidium concentrations were measured following an oral load of rubidium chloride. Eight patients receiving short-term digoxin therapy, 10 patients with chronic renal failure and 22 patients with untreated essential hypertension were studied, and the findings were compared with those in healthy control subjects matched for age, sex, race, obesity index, and plasma and red cell potassium concentrations. In patients receiving short-term digoxin therapy, and in patients with chronic renal failure, the increases in plasma rubidium concentrations after the oral load of rubidium chloride were significantly enhanced and the increases in red cell rubidium concentrations were significantly attenuated. These findings are consistent with a generalized reduction in Na+, K+-ATPase activity in vivo. In contrast, in patients with untreated essential hypertension the increases in both plasma and red cell rubidium concentrations following the oral load were significantly enhanced. These data do not support the hypothesis that essential hypertension is associated with reduced Na+, K+-ATPase activity in vivo, at least in the red cell.
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PMID:An in vivo study of cation transport in essential hypertension. 610 Jul 48

Twenty-two young normotensive male subjects, 12 with an established family history of essential hypertension, were put on a low-followed by a high-sodium diet. Plasma from each dietary period was tested for inhibitory activity on Na-K-ATPase using three different techniques: measurement of 22Na efflux rate, measurement of 3H ouabain binding characteristics and a bioluminescent adenosine triphosphate assay. The high-sodium diet was associated with a diminished ouabain-sensitive sodium efflux rate constant in the whole group; however, no circulating inhibitor could be detected in the plasma. Those with and those without a family history of essential hypertension were indistinguishable. The results suggest that young normotensive individuals with a genetic predisposition to essential hypertension do not produce a circulating inhibitor of sodium-potassium adenosine triphosphatase (Na-K-ATPase) in response to a high-sodium challenge.
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PMID:Effects of changes in dietary sodium intake on normotensive subjects with and without a genetic predisposition to essential hypertension. 610 Jul 52

Fifty-three patients with mild to moderate essential hypertension were treated with enalapril (10-40 mg q.d.) alone, in combination with a fixed dose of hydrochlorothiazide (50 mg/day), or in a randomized cross-over study with varying dosages of hydrochlorothiazide (50, 25, 12.5 mg/day). Normalization of blood pressure was obtained in 47% of the patients after enalapril. In the remaining patients, all except four were normalized by the combination with hydrochlorothiazide. The addition of hydrochlorothiazide was required in six patients who had optimally responded to enalapril during the first three months. In the cross-over study, diastolic blood pressure was maintained below 95 mmHg with all the doses of diuretic used in association with 40 mg enalapril. No adverse metabolic (blood glucose, cholesterol, triglycerides), renal (creatinine clearance, urinary lysozyme and gamma-GT) or haematological (total and differential counts) effects were observed after long-term treatment for one year with enalapril alone or in combination with hydrochlorothiazide. Blood uric acid decreased significantly after enalapril and tended to increase after the combination with hydrochlorothiazide. Enalapril increased Na/K ATPase activity on erythrocyte membranes thus reducing intracellular sodium and increasing potassium.
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PMID:Long-term antihypertensive, metabolic and cellular effects of enalapril. 610 Aug 70


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