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)

Investigations were carried out on the behavior of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) in essential hypertension (EH) under exogenous administration of synthetic ACTH and insulin. 40 stable EH patients and 21 normal subjects were included in the study. The increase (12-fold basal values) in plasma 18-OH-DOC in normal subjects under Tetracosactide was significantly higher than cortisol (4-fold basal values). Furthermore, insulin hypoglycemia increased 18-OH-DOC levels 5-fold, whilst basal values of cortisol were increased 2-fold. An increase in 18-OH-DOC and cortisol was also observed in EH patients: in the subgroup with normal and low plasma renin activity, however, the rise in these two steroids was significantly lower than in normal subjects both under Tetracosactide and insulin. No significant hormonal modifications were observed after furosemide administration either in the normal subjects or in the EH patients. 18-OH-DOC by itself does not, therefore, appear to play a pathogenetic role in EH.
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PMID:18-hydroxy-11-deoxycorticosterone response to ACTH, insulin and furosemide administration in essential hypertensive patients. 627 57

The effects of the converting enzyme inhibitor, SQ 14,225, on the renin-angiotensin system, adrenal function and blood pressure were investigated in 14 hypertensive patients, i.e., 10 with essential hypertension (EH) and 4 with renovascular hypertension (RVH). The mean blood pressure (MBP) and plasma aldosterone showed significant decreases in the EH with normal renin (NR) group and in the RVH group but no significant changes in the EH with low renin (LR) group. Plasma renin activity (PRA) increased significantly in the EH and NR group and in the RVH group but showed no significant change in the EH with LR group. Significant correlations were found between the fall in MBP after SQ 14,225 treatment and the pretreatment levels of PRA or plasma aldosterone. In an ACTH infusion study, the response of plasma aldosterone to ACTH revealed significant decreases after SQ 14,225 administration. In an angiotensin II (A II) infusion study, the response of plasma aldosterone was unchanged after SQ 14,225 administration. However, the pressor responses to A II infusion with SQ 14,225 were significantly higher than those without SQ 14,225. From these findings, it is concluded that the antihypertensive mechanism of SQ 14,225 may be due mainly to the decrease in levels of endogenous A II and that the reduction in plasma aldosterone after SQ 14,225 were significantly higher than those without SQ 14,225. From these findings, it is concluded that the antihypertensive mechanism of SQ 14,225 administration may be due to reduction of endogenous A II levels by converting enzyme inhibition.
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PMID:Effects of angiotensin I converting enzyme inhibitor (SQ 14,225) on the responses of blood pressure and steroid hormone to angiotensin II and ACTH infusion in hypertensive subjects. 627 73

The effect of potassium loading on plasma adrenocortical hormones concentrations in 9 patients with essential hypertension (EH) was investigated. The plasma renin activity (PRA), plasma concentrations of growth hormone (GH), ACTH, cortisol, deoxycorticosterone (DOC), 18-hydroxy-deoxycorticosterone (18-OH-DOC) and aldosterone, and serum electrolytes were measured before and after potassium chloride (KC1) infusion (0.33 mEq/kg/h, for one hour). The KC1 infusion caused significant increases in serum potassium levels and plasma levels of GH, ACTH, cortisol, DOC, 18-OH-DOC and aldosterone, while PRA remained unchanged. Regression analysis at 30 min revealed significant positive correlations between delta ACTH and delta cortisol, between delta ACTH and delta DOC, between delta ACTH and delta 18-OH-DOC. However, the relationship between delta ACTH and delta aldosterone was not statistically significant. These results suggest that (1) acute potassium loading causes a significant increase in the plasma ACTH level and increased levels of adrenocortical hormones may be produced by increased ACTH secretion, and (2) it may be considered that a part of the increased level of plasma aldosterone following acute potassium loading may arise from increased ACTH secretion in EH.
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PMID:Response of plasma ACTH and adrenocortical hormones to potassium loading in essential hypertension. 628 90

Alterations in the concentration of plasma dehydroepiandrosterone sulfate (DHEA-S) and cortisol in patients with essential hypertension (EH) were investigated. The subjects were 25 patients with EH: 7 of low plasma renin activity (PRA) group, 10 of normal PRA group and 8 of high PRA group; 7 normal subjects were used as the controls. Plasma DHEA-S and cortisol were measured before and after the following tests: (1) circadian rhythm (6:00, 16:00 and 24:00), (2) furosemide (0.7 mg/kg) test, (3) ACTH (12.5 IU/4 hr) infusion test, (4) dexamethasone (1.0 mg) test, (5) furosemide (0.7 mg/kg) test under dexamethasone (1.0 mg) treatment, (6) metopirone (1.5 g) test, (7) angiotensin II (8 ng/kg/min, 30 min) infusion test and (8) saline (1000 ml/hr) test. The alterations of the endogenous ACTH-adrenal hormone system as well as the renin-angiotensin-aldosterone system induced by these tests did not cause significant changes of plasma levels of DHEA-S in the 3 groups with EH. However, significant enhancement of plasma DHEA-S was observed after both the administration of exogenous ACTH and angiotensin II. It is considered that the responsiveness of DHEA-S to ACTH may increase in the low and normal PRA groups and that the responsiveness of DHEA-S to angiotensin II may increase in the high PRA group. Based on these results, it is suggested that plasma DHEA-S hardly or only partially participates as a causal factor of EH.
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PMID:A study on dehydroepiandrosterone sulfate in patients with essential hypertension. 628 91

Relationships between hormonal and hemodynamic parameters were examined during emotional stress in normal subjects and patients with essential hypertension. Plasma renin activity, aldosterone, cortisol concentration in the plasma and ACTH level, urinary catecholamine excretion were assayed, and arterial blood pressure, heart rate, ECG were recorded in 29 normal controls and 39 hypertensive patients before and after exposure to emotional stress. The findings were processed using the cluster technique of multivariable statistical analysis. Emotional stress was shown to produce more correlations in the system of hormonal balance compared to resting conditions, the interhormonal correlations being more pronounced in hypertensive patients as compared to normal controls. Stress-induced hypertensive response was shown to be achieved via different means: predominantly sympathoadrenal activation in normal subjects and the activation of renin-angiotensin-aldosterone system in hypertensive patients.
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PMID:[Relation between hormonal and hemodynamics indices during emotional stress in healthy individuals and in hypertensive patients]. 630 27

The hypertensinogenic effects of 19-hydroxyandrostenedione (19-OH-A-dione), which we reported as an amplifier of the action of aldosterone on the basis of the results obtained in bioassays using adrenalectomized rats, were evaluated in intact rats with both adrenals and kidneys. The administration of 19-OH-A-dione to the rats caused sodium retention and the 19-OH-A-dione treated rats developed high blood pressure, suppressed plasma renin activity and low plasma aldosterone, corticosterone and deoxycorticosterone concentrations. The hypertensinogenic potency of 19-OH-A-dione was incomparably higher than that of DOCA. The results indicate that 19-OH-A-dione is a potent hypertensinogenic steroid and causes the hypertensive state similar to mineralocorticoid excess. The evaluation of 19-OH-A-dione concentrations in human plasma revealed that 19-OH-A-dione is present in human peripheral circulation. It appears to be secreted by the adrenal cortex under the control of ACTH and the renin-angiotensin system. Plasma 19-OH-A-dione concentrations in patients with normal renin essential hypertension and low renin essential hypertension are higher than those in control subjects. 19-OH-A-dione is a newly recognised hypertensinogenic steroid in man.
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PMID:19-Hydroxyandrostenedione: a potent hypertensinogenic steroid in man. 631 Feb 35

Abnormalities in sodium metabolism, including the presence of endogenous circulating digitalis-like sodium transport inhibitors, have been implicated in the genesis of essential hypertension. Digitalis has also been reported to affect adrenal steroid output in vitro. We studied the effects of 4 days of treatment with the digitalis glycoside digoxin upon blood pressure, the renin-aldosterone axis, and pressor and steroidogenic responses to graded norepinephrine, angiotensin, and ACTH infusions in six normal men after pretreatment with dexamethasone. Digoxin produced no significant changes in blood pressure, urinary electrolyte or aldosterone excretions, PRA or aldosterone concentrations, or the incremental responses of aldosterone or cortisol to angiotensin or ACTH. However, digoxin significantly augmented pressor responsiveness to both norepinephrine and angiotensin without significantly affecting the steady state baroreceptor-heart rate reflex. These findings support the hypothesis that digitalis-like factors may have important effects upon arterial blood pressure control in man.
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PMID:Effects of digoxin on responsiveness to the pressor actions of angiotensin and norepinephrine in man. 631 64

In view of recent evidence that spironolactone may inhibit synthesis of corticosteroids by a direct effect on the adrenal cortex, adrenocortical function was studied in eight patients with essential hypertension who had been treated with spironolactone from 3 months to 14 years. Their 24 h renal excretion of adrenocorticoid metabolites and the responses of cortisol, aldosterone and 18-hydroxy-11 -deoxycorticosterone (18-OH-DOC) to an incremental infusion of tetracosactrin (1-24 ACTH) were compared with those in eight patients with recently diagnosed essential hypertension who had received no spironolactone. The spironolactone-treated group had a significantly higher excretion of aldosterone, whilst the excretion of other adrenocorticoid metabolites did not differ. The same group also required less tetracosactrin to stimulate a detectable rise of plasma cortisol and 18-OH-DOC, they had greater plasma 18-OH-DOC responses at all infusion rates and, at the lowest infusion rates, had greater aldosterone responses. These results indicate that long-term spironolactone therapy does not inhibit adrenocortical function and may have some stimulatory effects.
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PMID:Long term spironolactone and the adrenal cortex in essential hypertension. 721 21

Although propranolol administration produces a lowering of PRA, PAC does not decrease in a similar fashion. In the present study the effects of propranolol on the aldosterone MCR were examined. Eight patients with essential hypertension were studied while receiving treatment with a diuretic and again after propranolol (160 to 320 mg/day) was added to the therapeutic regimen. Propranolol therapy was associated with a 25% decrease in PRA (p less than 0.05) and changes in PACs that were variable but not significantly different from diuretic therapy alone. The aldosterone MCR decreased from 1420 +/- 120 to 1120 +/- 90 L/24 hr in response to propranolol (p less than 0.01). The average production rate of aldosterone (MCR X PAC) did not change after propranolol treatment despite a decrease in PRA. There were no changes in plasma concentrations of potassium or in ACTH secretion (as reflected by levels of cortisol) to explain a role for propranolol to sustain aldosterone secretion. Thus propranolol administered to hypertensive patients pretreated with a diuretic can affect circulating levels of aldosterone apart from changes in PRA. Propranolol therapy produces a moderate reduction in aldosterone MCR and appears to augment aldosterone production by a mechanism exclusive of known stimuli.
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PMID:Effects of propranolol on aldosterone plasma concentration and aldosterone metabolic clearance in hypertensive patients. 736 15

Increased levels of progesterone in serum have been reported in male patients with essential hypertension (EH). We, therefore, investigated serum progesterone levels in relation to excretion of aldosterone after 4 days of low Na+ intake and 6 days following high Na+ diets, in 11 normotensive controls, 22 male patients with EH and 8 male patients with hypertension of renal origin (RH). In the group of normotensive controls, the concentration of progesterone in serum averaged 228 +/- 90 and 186 +/- 93 (mean +/- SD) pg/ml during low and high regimens of Na+ intake, respectively, despite a fall in the excretion of aldosterone from 22.8 +/- 9 to 1.8 +/- 1.4 microgram/24 h. Similarly, in patients with EH, serum progesterone remained unchanged during either low or high Na+ intake regimens: 197 +/- 73 and 219 +/- 83 pg/ml, respectively. In patients with RH, serum progesterone tended to be lower during both low and high Na+ diets: 167 +/- 61 and 185 +/- 72 pg/ml, respectively. In 5 normotensive controls, diurnal variations of progesterone and cortisol were significantly correlated (r = 0.726, p < 0.005). The results of the present study suggest, that progesterone is not involved in metabolism of Na+, either in normotensive or hypertensive male subjects. Correlation between circadian variations of progesterone and cortisol suggests, that progesterone levels are modified by ACTH secretion.
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PMID:Regulation of serum-progesterone in patients with essential hypertension. 743 15


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