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

To determine whether defective calcium-efflux pump activity may be responsible for calcium overload in platelets from patients with essential hypertension, the properties of a calmodulin-stimulated Ca(2+)-ATPase in membranes from 25 normotensive and 27 hypertensive subjects were compared. Calcium-ATPase did not differ in affinity for calmodulin or Ca2+ between groups. Stimulation of Ca(2+)-ATPase activity at saturating calmodulin concentrations is diminished in calmodulin-deficient membranes from established essential hypertensive patients (64%) compared with normotensive subjects (125%) (P < 0.01). The capacity for Ca(2+)-ATPase activity (basal and calmodulin-activated) is markedly greater (1.5 to 1.8-fold) in both native and calmodulin-deficient platelet membranes from hypertensive compared with normotensive subjects. The data suggest that calmodulin-stimulation of Ca(2+)-ATPase in platelets from patients with established essential hypertension does not effectively maintain Ca2+ homeostasis, and that the increased Ca(2+)-ATPase capacity may reflect an adaptation to increased intracellular calcium concentration.
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PMID:Platelet membrane Ca(2+)-ATPase: blunted calmodulin-stimulation in essential hypertension. 285 41

Basal electric potential in the plasma membrane of synaptosomes and platelets as well as the membrane potential in erythrocytes is lower in spontaneously hypertensive rats than in normotensive animals. Similar potential alterations have been found in platelets and erythrocytes of essential hypertensive patients. The reduction of the basal component of the transmembrane potential in synaptosomes and platelets in primary hypertension is partially or entirely compensated by an increase of its electrogenic component as a result of an enhanced activity of Na+K(+)-ATPase. In erythrocytes of patients with renal hypertension and in Cushing's syndrome no alterations of membrane potential are observed.
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PMID:Evidence of lowered plasma membrane potential in different cell types in primary hypertension. 285 90

The activity of the ouabain-sensitive Na+K+-ATPase may be reduced in primary hypertension by an ouabain-like humoral factor with resultant increase in intracellular Na+ and Ca2+ and peripheral vasoconstriction. To test this, we studied the forearm blood flow in 18 normotensive subjects. First, nifedipine, phentolamine, prazosin, sodium nitroprusside and ouabain were infused into the brachial artery. Secondly, each vasodilator was given in combination with ouabain. Blood pressure was measured directly, and blood flow by venous occlusion plethysmography. When nifedipine was combined with ouabain the elevation of vascular resistance was completely abolished. We detected no effect on the forearm veno-arterial difference for noradrenaline following intra-arterial infusion of drugs. If an ouabain-like factor plays a role in producing the elevated resistance of chronic hypertension, calcium entry blockers will act close to the site of this primary abnormality.
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PMID:Ouabain-induced elevation in forearm vascular resistance, calcium entry and alpha-adrenoceptor blockade, and release and removal of noradrenaline. 289 70

We have studied sodium potassium ATPase activity, the effect of endogenous plasma on sodium pump activity, potassium permeability and intracellular sodium and potassium concentrations in normotensive subjects without (n = 36) and with (n = 33) a positive family history of hypertension, and in patients with untreated essential hypertension (n = 52). Sodium pump activity was studied as ouabain sensitive uptake of rubidium 86 in washed red blood cells, incubated in an artificial medium closely resembling the anorganic constituents of plasma. Any influence of endogenous plasma on sodium pump activity was investigated by re-incubating the washed red blood cells in their own plasma and comparing ouabain sensitive rubidium uptake in the two media. To correct for any possible differences in external potassium concentration, a function for the relation between extracellular potassium concentration and absolute transport rates was derived experimentally. From this, actual transport rates in plasma were corrected by computer to an extracellular potassium concentration of 4.0 mmol/l. Sodium pump activity, concentration of circulating sodium transport inhibitor, potassium permeability and intracellular electrolytes were not statistically different in subjects with and without a positive family history of hypertension. Hypertensives had significantly raised sodium pump activity in artificial medium, but not when red cells were re-incubated in their own plasma. Thus, endogenous plasma inhibited the sodium pump by between 12% and 15%. Hypertensives also had a significantly raised potassium permeability. Potassium permeability and sodium pump activity were correlated significantly. Intracellular sodium concentrations were similar in normotensives and hypertensives, but the later showed a significantly lower intracellular potassium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Raised sodium pump activity and a circulating sodium transport inhibitor demonstrated on red blood cells of patients with untreated essential hypertension: correlation of pump activity with potassium permeability. 298 7

Several reports indicate that erythrocytes (RBCs) from blacks and men have higher sodium concentrations than those from whites and women. One possible mechanism to explain this finding is a difference in the activity of Na+-K+-ATPase. To explore this possibility, we have studied the Na+ and K+ kinetics of RBC Na+-K+-ATPase and RBC Na+ and K+ concentrations in 37 normotensive blacks and whites, both males and females. The maximal initial reaction velocity (Vmax) values for RBC Na+-K+-ATPase were lower in blacks and men as compared with whites and women. Higher RBC Na+ levels were observed in blacks and males vs. whites and females. Significant inverse correlations were noted between the Na+-K+-ATPase activity and RBC Na+ concentrations. These findings indicate that cellular Na+ homeostasis is different in blacks and men as compared with whites and women. Since higher RBC Na+ concentrations have also been observed in patients with essential hypertension as compared with normotensive subjects, the higher intracellular Na+ concentrations in blacks and men may contribute to the greater predisposition of these groups to essential hypertension.
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PMID:Race and sex differences in erythrocyte Na+, K+, and Na+-K+-adenosine triphosphatase. 298 33

A simplified method for the determination of natriuretic factor in the urine as measured by digoxin-like substance was studied. Digoxin-like substance in the urine was estimated by RIA using anti-digoxin antibody after being extracted by reversed phase cartridge column but without gel filtration. The values found by radioimmunoassay (RIA) yielded a significant correlation with those of the inhibitory effect of Na-K-ATPase activity which was measured by biochemical assay as described by Hamlyn et al. Using this RIA method, the effect of salt intake on natriuretic factor in urine was studied in patients with essential hypertension. The natriuretic factor on a high sodium diet (NaCl 20 g/day for three days) increased approximately 1.5 times, as compared to those on a low sodium diet (NaCl 3 g/day) (p less than 0.05). The Natriuretic factor showed a positive correlation with urinary Na excretion (P less than 0.050) when the patients were placed on ad. lib. sodium diet. From these results, it is suggested that secretion of natriuretic factor in the urine might be regulated in part by salt intake.
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PMID:Effect of sodium intake on the excretion of urinary natriuretic factor in essential hypertensives. 299 16

ATPase activities were determined in haemolysed and dialysed erythrocytes and in haemoglobin-free membranes of twenty patients with essential hypertension and twenty normotensive controls. Ouabain-sensitive ATPase (Na-K-ATPase) activity of haemolysate but not that of membranes was decreased in hypertensives whereas ouabain-insensitive ATPase (Mg-ATPase + some residual Ca-ATPase) activity was increased in both enzyme preparations when measurements were preformed in the absence of Ca2+-chelating substances. In haemolysed erythrocytes ouabain-sensitivity as a percentage of total ATPase activity was a good discriminator between both groups and may be a possible marker for essential hypertension. The decreased activity of Na-K-ATPase in haemolysate is apparently due to a non dialysable inhibitor of Na-K-ATPase which is either tightly bound to the erythrocyte membrane or dissolved in the cytoplasm. Following haemolysis with subsequent centrifugation the Na-K-ATPase inhibitor is removed, at least in part, and thus differences in Na-K-ATPase activity demonstrable in haemolysed and dialysed erythrocytes are no longer apparent in haemoglobin-free membranes.
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PMID:Evidence for a Na-K-ATPase-inhibitor in erythrocytes of patients with essential hypertension. 299 50

A sensitive assay method to evaluate the inhibitor of Na+, K+-ATPase in human urine was developed by measuring the inorganic phosphate liberated from ATP in vitro using Na+, K+-ATPase from porcine cerebral cortex. Ouabain inhibited the Na+, K+-ATPase by competing with the potassium ion (an apparent Ki = 2.6 +/- 0.89 X 10(-8) M, n = 8) under the condition of 100 mM NaCl, 4.5 mM MgSO4 and 0.56 mM ATP. The apparent Km value of KCl was 0.4 mM. Factors inhibiting Na+, K+-ATPase were detected in the post-salt fraction on Sephadex G-15 chromatography following the ethanol extraction of lyophilized fresh urine of sodium loaded human subjects (300 meq Na+/day, for 4 days) with essential hypertension. Two active fractions around the 400 daltons following salt were eluted on Sephadex G-15 chromatography. The slower eluted factor competed kinetically with potassium ion, but the inhibitory activity was lost within two days during storage at 4 degrees C. The faster-eluted inhibitor lost its activity within a day. These results indicate that the unstable inhibiting factors of Na+, K+-ATPase exist in human urine and one of these factors inhibits ouabain sensitive Na+, K+-ATPase by binding to the potassium binding site (or very close to it), which exists at the outer surface of the cell membrane of this enzyme.
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PMID:Sensitive assay and kinetic property of urinary inhibitor of Na+, K+-ATPase in sodium-loaded patients with essential hypertension. 299 60

The effects of high sodium intake on erythrocyte 22Na efflux rate constants were studied in 25 patients with essential hypertension and 9 normal subjects. With changes in sodium intake from 100 mEq to 300 mEq/day, both total and ouabain sensitive 22Na efflux rate constants decreased significantly (p less than 0.001) in "salt-sensitive" patients (-0.031 +/- 0.005 and -0.035 +/- 0.006 /hr, respectively), but these responses were variable in "nonsalt-sensitive" patients and in normal subjects. The "salt-sensitive" patients showed a significant increase in their body weight, while intraerythrocyte sodium contents remained unchanged in the both groups. These results suggest that the abnormal change in membrane Na-K-ATPase activity may, at least in part, be involved in the mechanism of sodium susceptibility in patients with essential hypertension.
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PMID:Abnormal relationship between dietary sodium intake and red cell sodium transport in salt-sensitive patients with essential hypertension. 300 Jun 55

The plasma of normal man and the rat, and an acetone extract of hypothalamus from the rat, have an ability to inhibit Na-K-ATPase which is related directly to salt intake. The ability of the plasma to inhibit Na-K-ATPase is raised in essential hypertension. The ability of plasma and of an acetone extract of hypothalamus from six spontaneously hypertensive (SHR) rats and six normotensive control (WKY) rats to inhibit Na-K-ATPase of fresh guinea-pig kidney was studied using cytochemical bioassay techniques. With a validated assay, which measures the capacity of biological samples to stimulate glucose-6-phosphate dehydrogenase (G6PD) as an index of their capacity to inhibit Na-K-ATPase, the mean G6PD-stimulating ability of the plasma from the SHR and the WKY rat was 772.3 +/- 48.1 units/ml and 12.5 +/- 2.6 units/ml respectively (P less than 0.01) and of the hypothalamic extracts it was 2.2 +/- 1.7 X 10(8) and 4.5 +/- 1.8 X 10(4) units/hypothalamus (P less than 0.01). With a semi-quantitative cytochemical assay, which measures Na-K-ATPase activity directly, plasma and an acetone extract of hypothalamus from the spontaneously hypertensive rat had much greater capacities to inhibit Na-K-ATPase than plasma and extract from the WKY rat. These raised levels of Na-K-ATPase inhibitory activity in the plasma of the SHR rat are similar to the highest values found in the plasma of patients with essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na-K-ATPase-inhibiting and glucose-6-phosphate dehydrogenase-stimulating activity of plasma and hypothalamus of the Okamoto spontaneously hypertensive rat. 300 23


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