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

The content of calcium bound to the erythrocyte membrane and the effect of intracellular calcium concentration on the activity of Na+, K+-ATPase in the reconstituted erythrocytes were studied in 20 patients with essential hypertension and in 20 individuals with normal pressure. In incubation of the erythrocytes in a solution containing EDTA much more calcium is removed from the outer surface of their membrane in patients with essential hypertension than in the control group (60 +/- 5 mEq/l and 41 +/- 3 mEq/l, respectively). When the intracellular calcium concentration varies from 0 to 500 mumol/l, which corresponds to a rise in the free calcium (Ca2f+-3) concentration to 41 mumol/l, a difference in the changes of Na+, K+-ATPase activity of the reconstituted erythrocytes is noted. When intracellular calcium concentration is 50 mumol/l (Ca2f+-3 mumol/l), ATP-ase activity in patients with essential hypertension is 21% less than that in individuals with normal pressure (P less than 0.005). The authors explain the difference in the kinetics of Na+, K+-ATPase changes by the different degree of calcium depletion of the inner surface of the erythrocyte membrane in relatively low Ca2f+ values in the internal medium. The data obtained are evidence of the altered calcium-binding capacity of the erythrocyte membrane, which may cause the increased permeability of the erythrocyte membrane to sodium and potassium ions in patients with essential hypertension, which the authors had revealed earlier. The authors consider the revealed changes to be a fragment of a more extensive membrane defect which may be the principal cause of activation of the servomechanisms which maintain arterial pressure.
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PMID:[Role of membrane-bound calcium in the changes of ion permeability and Na+, 5+ and ATPase activity of the erythrocytes in hypertension]. 14 18

Twenty-one male children and 3 male adults with essential hypertension were infused with physiological saline solution (15 ml/kg/hr) for 1 hr after they had been supine for 90 min. The blood pressure and heart rate were monitored, and blood was taken twice before and after the infusion to measure the plasma Na-K ATPase inhibitor. After saline infusion, both the plasma Na-K ATPase inhibitor and blood pressure increased significantly in the hypertensive adults, and the number of Na pump sites decreased. However, such changes were not observed in the hypertensive children. These findings suggest that circulating Na-K ATPase inhibitor may not appear following acute saline infusion in hypertensive children unlike in hypertensive adults, and that the mechanisms regulating cell membrane sodium transport and high blood pressure may differ between hypertensive children and adults.
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PMID:Significant difference in the effect of acute saline loading on plasma Na-K ATPase inhibitor and blood pressure between children and adults with essential hypertension. 131 74

The effect of chronic alcohol consumption on Na(+)-K+ ATPase, Na(+)-Li+ countertransport, outward Na(+)-K(+)-Cl- cotransport system and the Na+ leak was investigated in red blood cells from 18 normotensive subjects with a daily alcohol intake of more than 150 g. The study was repeated after 3 months of alcohol withdrawal, and results were compared with a group of 20 healthy normotensive teetotalers. Maximal efflux rate (Vmax) and apparent dissociation constant for internal Na+ (KNa) of the Na(+)-K+ pump and the Na(+)-Li+ countertransport were significantly higher in alcohol consumers. A positive correlation between daily alcohol intake and Vmax of both transport systems (p less than 0.05) was observed. These values significantly decreased after alcohol withdrawal. A simultaneous stimulation of the Na(+)-K(+)-Cl- cotransport system after alcohol withdrawal was also observed. Blood pressure values were higher in alcoholics (133.7/82.3) than in abstainers (121.4/75 mmHg) and significantly decreased (128.5/76.9 mmHg) after withdrawal. A positive correlation between the stimulation of the Na(+)-K(+)-Cl- cotransport and the decrease of blood pressure after withdrawal was observed. In conclusion, chronic alcohol intake induces disturbances on red blood cell Na+ metabolism that dissipate with the cessation of drinking. Similar abnormalities also reported in humans and animals with primary hypertension have been associated in the pathogenesis of essential hypertension. Therefore, the pressor effect of chronic alcohol intake could be mediated through these changes in cellular Na+ metabolism.
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PMID:Chronic alcohol intake induces reversible disturbances on cellular Na+ metabolism in humans: its relationship with changes in blood pressure. 132 3

A total of 116 subjects with borderline hypertension, 67 relatives of normotensive probands and 29 relatives of hypertensive probands were examined. The activity of Na,K-ATPase in the red blood cells and pulmonary hemodynamics were studied by kinetocardiography. The normotensives with a family history of essential hypertension and subjects with borderline hypertension were found to have elevated pulmonary systolic pressure. The changes were coupled to lower erythrocyte Na,K-ATPase activity, which seems to suggest that endogenous ouabain-like factor that inhibits the enzymatic activity is present in plasma.
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PMID:[Na K ATPase activity and pulmonary hemodynamics in the development of arterial hypertension]. 132 43

To evaluate the antihypertensive and hormonal effects of oral magnesium supplementation, 17 inpatients with untreated, uncomplicated mild-to-moderate essential hypertension (EH) and 8 age-matched normotensive controls (controls) were given MgO orally 3 times a day at a daily dose of 1.0 g (0.6 g per day as Mg) for a period of 2 weeks. Supplementation of MgO elicited a significant fall in averaged mean blood pressure calculated with a 24-h ambulatory blood pressure monitoring system (MBP) in EH from a baseline value of 104.3 +/- 12.2 to 99.5 +/- 11.6 mmHg (p < 0.05), while controls remained unaltered from a baseline value of 85.1 +/- 11.5 to 84.5 +/- 13.3 mmHg. The percentage reductions in systolic and diastolic blood pressures were similar during daytime and nighttime in EH. According to the extent of reduction in MBP with magnesium supplementation, EH patients were divided into 2 groups, responder and nonresponder. The level of plasma renin activity (PRA) in the responder group was significantly higher than that of the nonresponder group (p < 0.05). After 2 weeks of magnesium supplementation, the plasma level of Na+, K(+)-ATPase inhibitory activity (PATPI), defined as equivalency to ouabain, was reduced significantly from 0.75 +/- 0.54 to 0.40 +/- 0.30 mumol ouabain/ml (p < 0.05) in the responder group, while it remained unaltered in controls and the nonresponder group. PRA, plasma aldosterone concentration, urinary epinephrine and norepinephrine excretion, and urinary sodium excretion did not change significantly in either control subjects or EH (responder and nonresponder groups). A significant negative correlation existed between the pretreatment PRA and changes in MBP after magnesium supplementation in EH (r = -0.65, p < 0.01), and there was a significant positive correlation between changes in PATPI and changes in MBP as a whole (r = 0.41, p < 0.05). These results support the view that oral magnesium supplementation is a useful approach to treatment of patients with uncomplicated essential hypertension, especially those with high plasmas renin activity. It appears that magnesium suppresses circulating Na+,K(+)-ATPase inhibitory activity to attenuate vascular tone, and thereby reduces blood pressure in EH.
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PMID:Effects of dietary magnesium supplementation on diurnal variations of blood pressure and plasma Na+, K(+)-ATPase activity in essential hypertension. 133 97

A crucial role of humoral factors in the pathogenesis of primary hypertension is discussed. In 1982 Hamlyn et al demonstrated the presence of a Na+, K(+)-ATPase inhibitor in the plasma of essential hypertensives and showed a significant correlation of the Na+, K(+)-ATPase inhibition with the blood pressure. In this study we examined whether an Na+, K(+)-ATPase inhibitor could be found in the blood of essential hypertensives as compared to patients with secondary hypertension (renal hypertension, renal artery stenosis, pheochromocytoma). Second, the possible correlation between an inhibition of Na+, K(+)-ATPase and the intracellular electrolyte composition was examined. The results demonstrate a similar reduction of Na+, K(+)-ATPase inhibition in both essential hypertensives and secondary hypertensives as compared to normotensive controls. Further, the intracellular electrolyte composition (Na+, Na; K+, Ca) does not show a significant correlation to the degree of Na+, K(+)-ATPase inhibition, whereas a significant correlation between the degree of Na+, K(+)-ATPase inhibition and intracellular Cl- concentration could be demonstrated. The present study shows that an endogenous Na+, K(+)-ATPase inhibitor is also present in secondary forms of hypertension, thus implying that a specific role in the pathogenesis of primary hypertension for an Na+, K(+)-inhibitor is unlikely.
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PMID:Na+, K(+)-ATPase inhibition and intracellular electrolyte content in essential and secondary hypertension. 164 95

Digoxin like immunoreactive factor (DLIF), has been implicated on the effect of sodium in essential hypertension. The different concentration of DLIF as a function of sodium intake was demonstrated in animal experience by some authors. In this work the urinary DLIF excretion is evaluated by RIA and its biological activity by Na+/K+ ATPase inhibition, in 5 urine samples at the end of a free sodium diet week and in 10 urine samples in the last day of a week with 250 mg sodium diet. The urinary DLIF excretion after the free sodium diet week was 0.3460 +/- 0.055 and at the end of sodium restriction diet week of 0.2910 +/- 0.061 nmol/l. Although the DLIF values in the sodium restriction week were smaller than the DLIF values of the free sodium diet week, there was no statistical difference (p = 0.113). In five patients the DLIF could be evaluated at the end of the first and second weeks without changes in the hypertensive therapeutics, with clonidine and nifedipine, along the two weeks. In these five patients at the end of the free sodium diet week and at end of the sodium restricted diet week were 0.3460 +/- 0.055 and 0.2780 +/- 0.060 nmol/l. The reduction of urinary DLIF excretion in the sodium restricted diet week, was significative (p = 0.020). The results of the Na/K ATPase inhibition in the same five patients were: 34.6 +/- 6.51% at the end of the free sodium diet week and 31.7 +/- 6.32% at the end of the sodium restricted diet week, the differences were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Determination of endoxin in hypertensive patients]. 164 7

Endogenous digital-like substance (DLS) is increased in patients with essential hypertension and is hypothesized to play a role in the pathogenesis of high blood pressure. Whether an increase in DLS in diabetic patients with hypertension is associated with a family history of hypertension or diabetic nephropathy was investigated. Plasma DLS was measured as Na(+)-K(+)-ATPase inhibitory activity (ATPI) in 100 Type 2 diabetic patients. Ouabain was used as a standard of Na-K-ATPase inhibition. Diabetic patients with hypertension demonstrated a greater ATPI level than normotensive diabetic patients (p less than 0.05). In patients with hypertension groups, the positive family history group had a higher ATPI level than the negative family history group (p less than 0.01). Microalbuminuria was not correlated with the ATPI level in diabetic patients. These results suggest that ATPI might play a role in the pathogenesis of hereditary hypertension associated with diabetes mellitus, but not have etiologic significance in diabetic nephropathy.
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PMID:Elevated endogenous digitalis-like substance in hypertensive diabetic patients with a family history of hypertension. 165 64

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.
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PMID:Erythrocyte membrane ouabain-sensitive Na+, K(+)-ATPase of hypertensive Nigerians. 165 90

Intracellular sodium concentration and Na+/K(+)-ATPase activity were studied in erythrocytes obtained from members of 14 families with one hypertensive parent and from age-matched control subjects, as part of a study on the genetic and environmental determinants of essential hypertension. We found reduced Na+/K(+)-ATPase activity, increased intracellular Na+ concentration, and reduced urinary Na+ excretion in hypertensive patients as compared with the control subjects. In the offspring of hypertensive parents an increase in intracellular Na+ concentration and a decrease in Na+/K(+)-ATPase activity were observed, with a significant correlation relating such parameters. Normotensive spouses did not differ from the normotensive control adults in any of the parameters studied, suggesting no influence of shared family environment in our family group. These data suggest that there is a strong genetic influence contributing to familiar alterations in cation transport, although long-term studies are needed to evaluate the influence of environmental determinants.
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PMID:Sodium metabolism in offspring of hypertensive parents. 165 91


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