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

Studies were undertaken to determine if the dissociation of aldosterone and plasma renin activity in low-renin essential hypertension is due to altered adrenal responsiveness to angiotensin II. The responsiveness of the adrenal glands to angiotensin II was determined by infusing graded doses of angiotensin II into normal subjects and into patients with essential hypertension and measuring changes in levels of plasma aldosterone in response to the infusion. To minimize the influence of endogenous angiotensin II and ACTH, supplemental sodium and dexamethasone were given before the infusions. Levels of plasma aldosterone and plasma renin activity were determined in normal subjects and in the same patients after the combined stimuli of furosemide and upright posture, a maneuver used to increase the level of endogenous angiotensin II. To determine if the changes in levels of plasma aldosterone during infusion of angiotensin II were due to alteration of the metabolic clearance of aldosterone, the metabolic clearance of aldosterone was measured before and during the infusion of angiotensin II. After sodium loading, dexamethasone treatment, and supine posture, levels of plasma aldosterone of normal subjects and patients with essential hypertension were suppressed equally. In response to the infusion of angiotensin II, the levels of plasma aldosterone of patients with low-renin essential hypertension were significantly higher than those of normal subjects or of patients with normal-renin essential hypertension. After furosemide and upright posture, levels of plasma aldosterone of patients with low-renin essential hypertension were significantly higher than those of patients with normal-renin essential hypertension, despite a blunted response in plasma renin activity of the patients with low-renin essential hypertension. Decreases in metabolic clearance of aldosterone during infusion of angiotensin II were similar in patients with normal-renin essential hypertension and in patients with low-renin essential hypertension and accounted for only a small fraction of the marked increase in levels of plasma aldosterone of patients with low-renin essential hypertension. It is concluded that patients with low-renin essential hypertension have increased adrenal sensitivity to angiotensin II. This increased sensitivity may explain the dissociation of aldosterone and plasma renin activity in low-renin essential hypertension.
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PMID:Increased adrenal sensitivity to angiotensin II in low-renin essential hypertension. 65 8

Overall 146 females suffering from essential hypertension (borderline, stage I and II according to WHO, 1980) were examined for basal concentrations of estradiol, estriol, progesterone, testosterone, cortisol, ACTH, prolactin in plasma, LH and FSH in blood and urine. The patients and 69 control normotensive females were reproductive, premenopausal, menopausal, postmenopausal, postcastration. Latent hypertension was elicited at bicycle exercise. It was found that relationships between sex hormones and gonadotropins both in hypertensive and normotensive women did not differ noticeably in reproductive period and in menopause. Hormone defects due to primary and secondary infertility, castration, menopause did not raise the risk of arterial hypertension onset. An-Unfavorable course of hypertension was observed in premenopause, following operative castration, in climacteric syndrome. The severity of AH at reproductive age was associated with hyposecretion of progesterone, estrogens and gonadotropins LH, FSH. This relationship was absent in menopausal women. A conclusion is proposed on miner significance of sex hormones imbalance and gonadotropins in the onset of arterial hypertension in females varying by generative activity.
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PMID:[Role of imbalance of sex hormones and gonadotropins in the development and course of essential hypertension in women]. 132 46

19-hydroxy-androstenedione (19-OH-A), a C19 steroid, is an amplifier of the sodium retaining action of aldosterone under the control of ACTH and renin-angiotensin system. These findings suggest that 19-OH-A may be involved in the regulation of hydroelectrolyte balance and blood pressure. Aim of the present study was to examine the behaviour of 19-OH-A in normal volunteers (N) and in patients with Essential Hypertension (EH) in basal conditions and after dynamic tests such as postural changes, physical exercise and ACTH administration. The significant increase in 19-OH-A after ACTH confirms its adrenal origin. During bicycle exercise the significant increase in plasma catecholamines, renin-activity, aldosterone, blood pressure and heart rate at maximum effort was not associated with a parallel increase in 19-OH-A. No significant differences were found in plasma 19-OH-A levels between N and EH patients both in basal conditions and after dynamic tests. Therefore, our findings seem to exclude an important role of 19-OH-A in the pathogenesis of EH.
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PMID:Plasma 19-hydroxy-androstenedione (19-OH-A) in essential hypertension. 133 Mar 85

Thirty-five stage I-II essential hypertension subjects aged 25-63 were examined after the 1st and 10th acupuncture to clarify the effect of a single procedure and a course of acupuncture treatment on blood ACTH, STH, TTH, beta-endorphine, neurotensin, thyroxine, aldosterone, hydrocortisone and plasma renin activity. The hormonal spectrum was determined by radioimmunoassay using special kits. The blood was obtained before acupuncture, 5 min after introduction of the needles, immediately and 30 min after their removal. It is shown that acupuncture-related decline of arterial pressure occurs in participation of pituitary and adrenal hormones as well as polypeptides beta-endorphine and neurotensin.
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PMID:[The effect of acupuncture on endocrine regulation in hypertensive patients]. 164 16

The episodic secretion of aldosterone depends on the dietary sodium intake, alterations in posture and follows ACTH circadian rhythm. Aldosterone daily profiles have been studied in 23 supine essential hypertensive patients on normal sodium intake. Secretory pulses at a frequency of two to five pulses per 12 hr have occurred, independent of PRA levels. Among 13 patients with normal PRA two lost pulsatility when sodium was loaded (10 g/24 hr) and the same happened with two others on sodium restricted diet (2 g/24 hr). These results suggest a profound effect of dietary sodium intake on the pulsatile pattern of aldosterone secretion, particularly in normal PRA essential hypertension.
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PMID:Daily profiles of aldosterone levels during normal, high and low sodium intake in patients with essential hypertension. 177 97

In this randomized, open-label trial, 24 subjects were studied. There were 12 subjects with essential hypertension and 12 normotensive controls who received, after an initial control period, 48 h of treatment with a transdermal estradiol patch or ketoconazole tablets every 8 h for six doses, or in combination. LHRH (100 micrograms) and ACTH (250 micrograms) were given at 48 h of each treatment. Each treatment was one week apart. In both normotensive and hypertensive men ketoconazole reduced adrenal and gonadal androgens, raised 11-deoxycortisol and 17 alpha-hydroxyprogesterone levels; blunted the rise of cortisol to ACTH and had no effect on the response of LH to LHRH. Transdermal estradiol raised serum estradiol levels, blunted the time to peak plasma concentration of LH to LHRH and produced a normal response to ACTH. Although baseline level of total and free testosterone and DHEA-S were lower in hypertensive men, the response of the pituitary (LH) to LHRH and adrenal axis with ACTH were similar in both normotensive and hypertensive men. Blood pressure was unaffected by any of the treatment interventions in either normotensive or hypertensive men. Although ketoconazole or transdermal estradiol reduce androgens, there was no evidence that this reduction in androgens was involved with the short term regulation of blood pressure in hypertensive men.
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PMID:The effect of ketoconazole and transdermal estradiol on serum sex steroid hormones levels. 216 34

Plasma 18-hydroxycorticosterone (18-OHB) and aldosterone responses to angiotensin II (AII) and ACTH were examined in 2 patients with a 18-OHB-producing tumor (18-OHBPT) versus those in 8 patients with a aldosterone-producing adenoma (APA), 7 patients with low renin essential hypertension (LREH) and 10 normal subjects. Plasma 18-OHB and aldosterone levels and the 18-OHB: aldosterone ratio were high in patients with an APA and normal in patients with LREH. In patients with a 18-OHBPT, plasma 18-OHB and aldosterone levels were high and normal, respectively, resulting in a 2-fold greater 18-OHB: aldosterone ratio than that in patients with an APA. Patients with an APA had a blunted response of plasma 18-OHB and aldosterone to AII and a supranormal response of these corticoids to ACTH. Patients with LREH had a supranormal response of plasma 18-OHB and aldosterone to AII and a normal response of these corticoids to ACTH. In patients with a 18-OHBPT the responses of both plasma 18-OHB and aldosterone to AII and ACTH closely resembled those in patients with an APA but not in patients with LREH. These data suggest that 18-OHBPT may be a variant of aldosteronomas, producing a large amount of 18-OHB and a small amount of aldosterone.
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PMID:Altered responses of plasma 18-hydroxycorticosterone and aldosterone to angiotensin II and adrenocorticotropin in patients with a 18-hydroxycorticosterone-producing tumor. 255 39

Measurements of blood plasma ACTH, hydrocortisone, STH, somatostatin, insulin, glucagon levels and plasma renin activity in 70 patients with borderline hypertension (BAH) and in 20 normal male subjects have revealed increased ACTH, hydrocortisone, and somatostatin levels, elevated plasma renin activity, and reduced STH and insulin levels in the patients. A possible role of the pressor hormone system activation in the pathogenesis of borderline arterial hypertension and in BAH transformation into essential hypertension is discussed.
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PMID:[Hormonal disorders in borderline arterial hypertension]. 257 58

As many as 52 patients with essential hypertension aggravated by circulatory failure were examined for the clinical, hemodynamic and neurohumoral parameters during furosemide stimulation. In elderly patients, the optimal vasodilatory dose of nifedipine amounted to 10 mg, that of verapamil to 40 mg per os or to 5 mg i.v. In patients with the stimulated activity of plasma renin, the concentration of plasma aldosterone remained unchanged. The plasma concentrations of ACTH and cortisol tended towards increase while vasopressin concentration dropped. Side effects could be frequently observed. Hemodynamic shifts appeared to be negative. During the first hour, forced diuresis was recorded. In patients with unstimulated plasma renin activity, plasma aldosterone concentration declined, whereas the concentrations of ACTH, cortisol and vasopressin rose. Side effects were less in number, the hemodynamic shifts were positive, and diuresis turned out 2-3 times less during the first hour than within the next 4 hours. It is suggested that the efficacy of the treatment with calcium antagonists can be predicted according to the magnitude of the hourly diuresis with regard to the type of hemodynamics.
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PMID:[The efficacy of calcium antagonists in circulatory failure in elderly patients with hypertension]. 262 43

Clonidine hydrochloride via the central nervous system lowers blood pressure, inhibits ACTH and catecholamine release, and stimulates growth hormone secretion. To evaluate the effect of this drug on the release of glucoregulatory hormones during hypoglycemia, we studied the responses to insulin-induced hypoglycemia (0.1 units/kg) in 10 patients with mild essential hypertension before and after treatment for 16 weeks with transdermal clonidine. Clonidine significantly lowered blood pressure, basal plasma norepinephrine levels, and epinephrine and renin activity but did not affect basal growth hormone concentrations. Clonidine significantly reduced the norepinephrine and epinephrine responses to hypoglycemia (norepinephrine AUC from 207 +/- 16 SE to 156 +/- 25 nmol/L/min, epinephrine from 157 +/- 28 to 99 +/- 29 nmol/L/min; both p less than 0.05) and increased the growth hormone response (AUC from 763 +/- 148 ng/min/ml to 1164 +/- 292 ng/min/ml; p less than 0.05) but did not affect the cortisol response or the magnitude or rate of glucose recovery from hypoglycemia. Thus transdermal clonidine has several effects on glucose counterregulatory hormones that do not significantly alter insulin sensitivity or impair recovery from hypoglycemia.
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PMID:Effect of transdermal clonidine on the endocrine responses to insulin-induced hypoglycemia in essential hypertension. 264 99


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