Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The activity and properties of Na,K-ATPase in erythrocytes and their membrane preparations (ghosts) from 34 subjects with borderline hypertension and 21 normotensive controls were studied. The Na,K-ATPase activity was found to be by 43% lower as compared to control group. No changes in the Na,K-ATPase activity were revealed in the ghosts of borderline subjects. This suggests that the plasma of borderline subjects contains an inhibitor of Na,K-ATPase. The plasma level of sodium pump inhibitor was measured in 21 borderline hypertensive subjects. It was found to be about 19% compared with the control group. These findings suggest presence of Na,K-ATPase inhibitor in the plasma of borderline subjects, which is likely to be involved in the development of hypertension.
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PMID:[The activity and properties of Na,K-ATPase in the erythrocytes and the Na-pump inhibitor in the plasma of subjects with borderline arterial hypertension]. 166 9

Erythrocyte Na, K-ATPase was examined for its activity and relation to the concentration of the complexon EDTA in 39 patients with arterial hypertension (AH), 12 subjects with borderline hypertension, and 18 normotensives. The ionic composition and deformability of erythrocytes were also studied. As compared to normotensives, the patients with Stage I AH displayed a significantly lower activity of erythrocyte Na, K-ATPase, which may suggest that there is an enzyme inhibitor in the blood of the patients. According to the enzyme activity, the patients with Stage II AH were divided into two subgroups: 1) those with a lower activity and 2) those with a higher activity than healthy subjects. The patients with a Stage II AH who showed a lower activity of Na, K-ATPase exhibited a more elevated erythrocyte sodium level, whereas those who had a high activity of the enzyme displayed a decreased erythrocyte deformability. In addition, a positive correlation between erythrocyte sodium concentrations and Na, K-ATPase activity, as well as erythrocyte deformability was found in normotensives, whereas a negative correlation was established in AH patients.
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PMID:[Ionic homeostasis and erythrocyte deformability in patients with primary arterial hypertension]. 217 12

The effects of different beta-adrenoceptor agonists and antagonists on plasma noradrenaline and potassium concentrations were studied in patients with borderline hypertension. Heart rate, arterial pressure and the heart rate corrected duration of total electromechanical systole (QS2I) were also measured. Infusion of the beta-adrenoceptor agonists isoprenaline (non-selective) and salbutamol (beta 2-selective), but not prenalterol (beta 1-selective) caused dose-dependent increments in plasma noradrenaline. Isoprenaline and salbutamol decreased plasma potassium dose-dependently. For a given effect on heart rate and QS2I the fall in potassium was less pronounced after prenalterol. The effects of isoprenaline were also studied after the beta-adrenoceptor antagonists propranolol, 320 mg day-1 for 1 week (non-selective) and atenolol, 100 mg day-1 for 1 week (beta1-selective). The effects of isoprenaline, when infused in equipotent chronotropic doses, on noradrenaline and potassium were not affected by atenolol, whereas they were completely abolished by propranolol. The rise in noradrenaline during beta-adrenoceptor stimulation could be explained by presynaptic facilitation of noradrenaline release. The fall in potassium probably reflects stimulation of Na-K-ATPase dependent transport of potassium into the cell. Both effects were seen after beta 2- but not after beta 1-adrenoceptor stimulation. Hypokalaemia and raised levels of noradrenaline are also known to occur under such stressful conditions as acute myocardial infarction, when circulating levels of the endogenous beta 2-adrenoceptor agonist adrenaline are high. Blockade of these effects by beta-adrenoceptor antagonists may contribute to the cardioprotective effect of these drugs. This warrants further consideration of the clinical significance of beta-blocker selectivity.
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PMID:Cardioprotection by blockade of beta 2-adrenoceptors. 613 69

The etiology of essential hypertension is still a matter of some speculation. Research concerned with pre-hypertensive mechanisms of human essential hypertension usually includes subjects with either borderline hypertension or with a positive family history of hypertension. High blood pressure and increased left ventricular mass are risk factors for cardiovascular disease in adults. Much information about hypertension and other coronary artery disease risk factors in children and adolescents has been collected in the past two decades, and during the last years new evidence has emerged which indicates that essential hypertension originates early in life. Several studies have suggested that children and adolescents born following hypertensive pregnancies may constitute a risk group for future hypertension. The present study addresses the question concerning the future cardiovascular risk in offspring of women who had hypertension during pregnancy. The subjects in the present study were also studied in the search for early pre-hypertensive mechanisms. Fifty-nine children were studied, their mean age being 12.6 years. Forty-two children were born to mothers who had hypertension during pregnancy and 17 children were born after normotensive pregnancies by mothers who remained normotensive at follow-up 7-12 years after pregnancy. Blood pressure was measured at rest and during physical exercise. Left ventricular mass was calculated from M-mode echocardiogram. Erythrocyte concentrations of sodium and potassium and Na-K-ATPase activity were determined. Perinatal and maternal characteristics were collected from hospital records for all deliveries. Twenty-nine males and 23 females, of the initially studied children, were reexamined after 5.6 years. The present study demonstrates that children whose mothers had hypertension during pregnancy and were hypertensive at follow-up had higher blood pressure than children born following normotensive pregnancies. A familial factor for hypertension was an independent determinant of blood pressure, but not a determinant of left ventricular mass. Children born following hypertensive pregnancies had lower birth weight, shorter gestational period and higher blood pressure at follow-up. There was no relationship between birth weight and blood pressure in these children, but there were associations between maternal blood pressure during pregnancy and birth weight as well as blood pressure at follow-up. The difference in blood pressure persisted as the children matured. Particularly the children whose mothers had hypertension during pregnancy and were hypertensive at follow-up maintained their rank with regard to blood pressure and left ventricular mass during adolescence.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Blood pressure and left ventricular mass in children and adolescents: the Hypertension in Pregnancy Offspring Study. 785 47