Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The number of sodium pump receptors in erythrocytes (maximum binding of ouabain to erythrocytes; Bmax) was examined in relation to a family history of essential hypertension (FH-HT), the body mass index (BMI), urinary sodium excretion and blood pressure in 71 normotensive children (13 to 15 years of age), and in relation to sodium intake in 6 children who had various kidney diseases but displayed a normal renal function (6 to 13 years of age). Bmax was significantly lower in children with FH-HT than in those without FH-HT. However, the BMI, urinary sodium excretion and blood pressure showed no significant differences between the groups. Bmax was not significantly different between the top 20% tile group of BMI or urinary sodium excretion and the bottom 20% tile group of BMI or urinary sodium excretion. Furthermore, Bmax was unchanged during and after restriction of sodium intake in children with nephropathy. These findings suggest that Bmax may be a genetic marker for essential hypertension, since it was suppressed regardless of the BMI or urinary sodium excretion in normotensive children with FH-HT, and since it did not change according to sodium intake in children with renal diseases.
 ...
PMID:Maximum binding of ouabain to erythrocytes in relation to a family history of essential hypertension, sodium balance and body weight in normotensive children. 133 78

The usefulness of salt restriction in essential hypertension is still now disputed. This study was designed to test the influence of a diet with and without salt restriction in 19 untreated essential hypertensives (12 with and 7 without family history of hypertension) and free of cardiovascular and renal complications. Each patient was examined after a placebo period, after 1 month of salt restriction, and after 1 month of salt supplementation. Weight, blood pressure, 24 hours urinary sodium excretion and red blood cell ionic fluxes were measured. In patients with hypertensive heredity, the blood pressure did not change. The intracellular sodium concentration, the cotransport and the countertransport remained stable. The ouabain sensitive sodium pump slightly increased during salt restriction and remained stable after salt supplementation. In patients without such hypertensive heredity (who were older and heavier), sodium restriction period was characterized by significant decrease in blood pressure, weight, intracellular sodium concentration and increase in sodium pump activity. When salt was increased, all the parameters remained stable. A more balanced diet with sodium restriction decreases the blood pressure in relation to age, weight and the blood pressure level. Hypertensive heredity does not seem to be a parameter of salt sensitivity. The blood pressure decrease is also related to the quantitative importance of sodium restriction. The ouabain sensitive pump activity changes during diet especially in relation to weight loss and decreasing salt intake.
 ...
PMID:[Effect of dietary sodium in hypertension not treated with drugs]. 133 57

The postulate of a natriuretic factor inhibiting the sodium pump in the kidney led to the detection of increased concentrations of endogenous digitalis-like factors in blood after salt loading, in essential hypertension, in pregnancy-induced hypertension and in chronic hypervolaemia. The recent isolation of ouabain or a close isomer thereof from human plasma and the demonstration of a compound similar if not identical to digoxin in adrenals and human urine shows that mammals like non-vertebrates and toads may synthesize cardiac glycosides in their adrenals and possibly in hypothalamus. The hypothalamus also forms other compounds of unknown structure which bind to the cardiac glycoside receptor site. The differential functions of endogenously formed ouabain and of a digoxin-like substance are unclear. The detailed knowledge of the physiological role of both endogenously formed cardiac glycosides in the regulation of blood pressure has still to be worked out.
 ...
PMID:Endogenous digitalis-like factors. 139 72

Twelve-hour urinary sodium excretion, the number of sodium pump sites (Bmax) and the Na/K flux ratio in erythrocytes were measured in 13 previously diagnosed hypertensive subjects. At the time of the study, six subjects were still hypertensive and showed a significantly lower Na/K flux ratio in erythrocytes than the remaining seven subjects who were normotensive. Bmax was also lower in the hypertensive group compared to the normotensive group, although this was not statistically significant. Urinary Na excretion did not show any significant difference between the two groups. These findings suggest that a cell membrane sodium transport defect may have a role in the development of essential hypertension in adult life.
 ...
PMID:Erythrocyte sodium transport at twenty-year follow-up of childhood hypertension. 158 Jan 52

An assessment of the ATPase functions of erythrocyte membrane of newly identified subjects having essential hypertension shows that Na+,K(+)-ATPase activity is higher in normal membranes than in membranes of individuals with essential hypertension. A study of the dependence of the enzyme on ATP in the presence of non-limiting concentrations of Na+ (120 mM) and Mg2+ (3 mM) shows that the pump in the membranes of hypertensive individuals, like that of normal humans, is easily saturable by ATP (greater than or equal to 2 microM). Analysis of the results of kinetic studies on the enzyme, in the presence of 5 mM K+, using the Hanes plot, reveals that, although the affinity (Km) of the pump for ATP is unaffected in essential hypertension, its maximum velocity (Vmax) is lower than in normal membranes. Even though the reason for a reduced sodium pump function in essential hypertension is not yet clear, it may not be unconnected with the presence of an endogenous inhibitor or with genetic or diet-induced membrane defects, as previously proposed by other workers in this area of research.
 ...
PMID:Erythrocyte membrane ouabain-sensitive Na+, K(+)-ATPase of hypertensive Nigerians. 165 90

Essential hypertension is characterized by polygenic inheritance and quantitative and/or qualitative abnormalities of membrane transport systems may function as intermediate phaenotypes. The present review attempts to evaluate the importance of sodium transport systems such as the sodium pump, cotransport and countertransport as aetiological or pathogenetic factors involved in primary hypertension. Furthermore, the relative importance of NaCl balance as an exogenous factor modifying these transport systems is reviewed. Controversial results exist with respect to the activity of the sodium pump and cotransport both as a function of blood pressure and NaCl balance. In contrast, accumulating evidence suggests that the activity of the counter-transport system is increased in essential hypertension and that this may be observed even before the elevation of blood pressure can be documented. In own studies performed in normotensive volunteers on a low (20 mmol/day) and high (320 mmol/day) NaCl intake, lymphocyte antiport activity was significantly higher during chronic NaCl loading. Therefore, alterations of the Na+/H+ antiport system may represent an intermediate phaenotype of gene(s) involved in the genesis of primary hypertension. Preliminary evidence suggests that NaCl balance may be an exogenous modulator of this system.
 ...
PMID:Membrane transport, sodium balance, and blood pressure regulation. 165 37

1. Using a Mulvany-Halpern myograph to measure changes in isometric tension, we have investigated the effect of ouabain on noradrenaline-induced contraction of human subcutaneous resistance arteries. 2. Low concentrations of ouabain (10 nmol/l or less) were shown not to alter vascular smooth muscle contractility or sensitivity to noradrenaline. 3. In contrast, higher concentrations of ouabain (100 nmol/l or more) were found to depress vascular smooth muscle contractility and to reduce the sensitivity of the noradrenaline concentration-response relationship. 4. These findings may have implications regarding the presence of an endogenous inhibitor of the sodium pump in essential hypertension and in pregnancy-associated hypertension.
 ...
PMID:Low-concentration ouabain does not inhibit noradrenaline-induced contraction of human resistance arteries. 165

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.
 ...
PMID:Roles of sodium, potassium, calcium, and natriuretic factors in hypertension. 193 82

The alteration of sodium ion transport in red blood cells was observed in SHR and patients with essential hypertension. The purpose of the present study was to determine the effects of dietary calcium intake on blood pressure and sodium ion transport of red blood cells in SHR. The SHR were fed a diet with three different levels of calcium contents as follows: 0.1% (low), 0.6% (normal) and 4.0% (high) of calcium between 6 and 20 weeks of age. At 20 weeks of age, the levels of erythrocyte sodium efflux, sodium or potassium contents in the red blood cells were measured. On the high Ca diet, SHR showed an attenuation of the increase in blood pressure. On the low Ca diet, SHR showed an enhancement of hypertension. In proportion of increasing of dietary calcium contents, SHR had a lower level of sodium content in the RBC and a higher activity of the sodium pump. However, the passive sodium permeability and sodium-potassium cotransport in SHR were similar among the three different Ca diets. It is concluded that the amounts of dietary Ca might be related to the regulation of blood pressure by changing the sodium pump of the cell membrane in SHR.
 ...
PMID:Effects of dietary calcium on erythrocyte sodium ion transport systems in spontaneously hypertensive rats. 195 55

Many membrane abnormalities have been described in human essential hypertension that may lead to an increased intracellular Na+ content, an example being reduced Na+ efflux by the sodium pump. We have previously found increased Na(+)-H+ antiport activity in leucocytes of hypertensive subjects. In the present study we examined the kinetics of this pump in 16 hypertensive and 20 carefully matched normotensive subjects by loading cells to different intracellular pH levels (as measured by fluorimetry) using a double-ionophore technique. The maximal rate of ethyl isopropyl amiloride-sensitive H+ efflux was significantly raised in leucocytes from the hypertensive subjects [75.3 +/- 6.2 versus 48.8 +/- 2.1 mmol/l per min in normotensives (mean +/- s.e.m.); P less than 0.001]. There was no difference in the affinity of the Na(+)-H+ antiport for intracellular H+. Intracellular buffering power at different internal pH levels in the range 6.0-7.1 did not differ in the two groups. We conclude that one reason for the reported intracellular alkalinity and increased sodium content of leucocytes from hypertensive subjects in bicarbonate-free media could be an increased number of active Na(+)-H+ exchangers or an increased turnover rate for each exchanger. A similar defect in vascular smooth muscle could account for the increased tone and thickening of the media. The abnormal maximal transport capacity of the leucocyte may be a useful membrane marker for future studies in human hypertension.
 ...
PMID:Kinetics of the human leucocyte Na(+)-H+ antiport in essential hypertension. 216 87


1 2 3 4 5 6 7 8 9 Next >>