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

Sixty-five patients with advanced chronic renal failure (CRF) but a normal extracellular fluid volume (ECFV), including 31 dialysis patients, were studied. Plasma volume, blood volume (BV), plasma renin activity (PRA), and mean arterial pressure were measured to examine whether hypertension (when present) is renin dependent, or whether it is related to an abnormal distribution of ECFV between the intra- and extravascular spaces. PRA was higher in dialysis than nondialysis patients, but the incidence of hypertension was the same. In both groups hypertensive patients with normal PRA and normotensive patients with elevated PRA were present. The patients were compared to 65 patients with essential hypertension (EH) and 56 normals. The BV and BV-to-interstitial fluid volume ratio were similar in these groups. We found no decreased BV in patients with EH as has previously been reported by others, possibly because we used an appropriate normalization index and matched control groups. In sum, hypertension in CRF patients with a normal ECFV cannot always be explained by elevated renin levels. In this respect, CRF patients resemble patients with EH. An abnormal extracellular fluid distribution does not seem to be involved in the maintenance of hypertension.
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PMID:Renin and blood volume in chronic renal failure: a comparison with essential hypertension. 354 11

In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations after the oral administration of rubidium chloride. In this paper we describe our findings in 22 patients with untreated essential hypertension, compared with the findings in 22 carefully matched control subjects. Our findings in patients receiving short-term digoxin therapy and in patients with chronic renal failure are also included for comparison. Whereas the findings in patients receiving digoxin and in patients with chronic renal failure are compatible with a widespread reduction in sodium, potassium-ATPase activity in vivo, the findings in patients with untreated essential hypertension are not. Further analysis of the data and a similar study of the disposition of 42K after the intravenous administration of 42KCl suggest that in vivo net cation transport is enhanced in the erythrocytes of patients with untreated essential hypertension.
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PMID:Cation transport abnormalities in vivo in untreated essential hypertension. 370 67

This study was realized to test De Wardener's hypothesis on the presence of a plasmatic and natriuretic factor in essential hypertension. By an indirect approach consisting of modification of plasma volume and sodium pool in chronic renal failure and primary hypertension with, at the same time, measurements of ionic flux variations in human erythrocytes, we provide some arguments to confirm the presence of such a factor in hydrosaline overloaded uraemic patients and in "salt-sensitive" essential hypertensive subjects.
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PMID:Effect of salt depletion on sodium ion transport from human erythrocytes. 399 42

The Na-K cotransport activity was measured in erythrocytes of 123 normotensive and 92 hypertensive patients, using the methodology described by Dagher and Garay. Large overlap of the values obtained in the two populations is observed, in such a way this laboratory test cannot be applied for the discrimination between primary and secondary hypertension. Moreover, the abnormalities described for the Na-K cotransport do not appear specific for primary hypertension. In this study, the influence of hypertensive heredity, but also obesity on this cotransport system could not be demonstrated. However, this transport activity is significantly decreased in patients with chronic renal failure, during treatment with oestro-progestatives or during the oestrogenic phase of the menstrual cycle. These data strongly suggest that the cotransport activity could be modified not only by the hypertensive familial predisposition but also by environmental and hormonal influences.
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PMID:The erythrocyte sodium-potassium cotransport in hypertensive patients: advantages and limitations. 400 62

The serum converting enzyme activity (SCEA) was measured in 86 healthy individuals (1.44 +/- 0.82 u, mean +/- SD), 39 patients with essential hypertension (1.53 +/- 0.71 u), 7 patients with hypertension due to renal artery stenosis (1.76 +/- 0.77 u), 14 patients with chronic renal failure (2.10 +/- 0.57 u), 7 patients with renal failure and hypertension (2.62 +/- 0.35 u), 22 normotensive pregnant women (1.02 +/- 0.26 u) and 6 hypertensive pregnant women (1.1 +/- 0.3). No difference was detected between men and women or between normotensives and hypertensives. However, a significant rise in SCEA was found in patients with chromic renal failure (P less than 0.005), in whom an enlarged pulmonary vascular bed and accelerated cellular breakdown are thought to be the causes of the elevated SCEA. During pregnancy, subnormal SCEA was found (P less than 0.005), and this is thought to be due to the enzyme consumption in the kinin system, which is activated during pregnancy. We assume that converting enzyme is not a limiting factor in angiotensin conversion, and most probably it does not contribute significantly to the pathogenesis of hypertension.
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PMID:Serum angiotensin converting enzyme activity in normal adults and patients with different types of hypertension. 609 66

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

In order to investigate the role and origin of serum angiotensin I-converting enzyme activity (ACEA) in hypertension, the correlation between serum ACEA and the renin-angiotensin-aldosterone system was evaluated in hypertensive patients of whom 36 had essential hypertension, five had hypertension associated with chronic renal failure, three had renovascular hypertension, and one had primary aldosteronism. Serum ACEA was 17.0 +/- 3.3 U (mean +/- sd) in the normotensive control, 20.1 +/- 7.1 U in patients with essential hypertension, 11.6 +/- 3.4 U in patients with chronic renal failure, 31.7 +/- 1.1 U in patients with renovascular hypertension, and 9.7 U in primary aldosteronism in a recumbent state. There was a significant correlation between serum ACEA and plasma renin activity (PRA) (r = 0.615, p less than 0.001, n = 45) and plasma aldosterone concentration (PAC) (r = 0.599, p less than 0.001, n = 34) in a recumbent state. However, there was no significant correlation between serum ACEA and mean blood pressure. Serum ACEA elevated with furosemide and an upright posture significantly correlated with elevation in PRA (r = 0.369, p less than 0.05, n = 32) but did not significantly correlate with elevation in PAC. It is suggested, therefore, that the kidney is the suspected source of the plasma activity of the enzyme and that serum ACEA plays a possible role in the regulations of blood pressure and electrolyte metabolism modulating the renin-angiotensin-aldosterone system.
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PMID:[The correlation between serum angiotensin I-converting enzyme activity and the renin-angiotensin-aldosterone system in hypertensive patients (author's transl)]. 627 8

Inhibitors of the Na+ pump have been proposed as participating in sodium excretion, extracellular fluid regulation, and in the rise of blood pressure. The presence of digitalis-like compounds in human plasma has been investigated by comparing the effects of plasma extracts to those of ouabain in 4 tests. - competition with ouabain for binding to the Na+ pump, - inhibition of Na+ and K+ dependent hydrolysis - inhibition of serotonin uptake by human platelets - central hypertensive effect Plasma fractions exhibited digitalis-like properties in the 4 tests. The effects of plasma extracts of 42 normotensive subjects (21 with family history of hypertension) and 38 patients with essential hypertension (15 with antihypertensive treatment) and 9 patients with chronic renal failure were compared. Plasma from Forty per cent of untreated hypertensive patients and normotensives with hypertensive heredity had a high inhibition level. Inhibition was enhanced in beta-blocker treated patients and decreased in those on diuretics. No digitalis-like activity was observed in uremic plasma. These observations strongly suggest the presence of digitalis-like compound(s) in human plasma and point to its possible association with hypertension.
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PMID:Circulating digitalis-like compounds in essential hypertension. 632 Oct 68

In order to clarify the role of the kallikrein-kinin system in the hypotensive mechanisms of converting-enzyme inhibition, captopril was administered in a single oral dose of 50 mg to 17 hypertensive patients, of whom 14 had essential hypertension, one had chronic renal failure, one had primary aldosteronism, and one had glucocorticoid responsive hyperaldosteronism. Captopril lowered blood pressure remarkably in either low-renin or normal-, and high-renin hypertensives, however, there was no significant relationship between the fall in blood pressure and pretreatment levels of plasma renin activity (PRA) in any of the patients any time after the administration. PRA was significantly increased in normal- and high-renin hypertensives but not in low-renin patients. Plasma aldosterone concentration (PAC) was decreased significantly in normal- and high-renin patients, while no significant change in PAC was observed in patients with low-renin activity. Captopril elevated plasma bradykinin concentration (PBK) from a control value of 12.5 +/- 4.1 (mean +/- s.d.) to 20.3 +/- 7.7 pg/ml (p less than 0.001) at 30 min, and there was a significant correlation between changes in PBK and changes in mean blood pressure 120 min after the administration in all the patients (r = 0.741, p less than 0.01, n = 17). In one patient with primary aldosteronism, PBK increased from a baseline of 10.0 to a maximum value of 19.0 pg/ml, corresponding to the rapid fall in blood pressure. Also, in one patient with glucocorticoid responsive hyperaldosteronism, captopril increased PBK from a control of 14.1 to 27.9 pg/ml at 30 min, corresponding to the marked fall in blood pressure from 170/106 to 136/90 mmHg. From these findings, it is suggested that the accumulation of kinins following captopril administration plays a major role in the short-term reduction of blood pressure in hypertensive patients, especially in those with low renin-angiotensin activity.
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PMID:[Acute antihypertensive effect of captopril in hypertensive patients: with special reference to kallikrein-kinin system]. 636 44


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