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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was shown in experiments on 200 albino rats that prolonged adaptation to the periodical effect of hypoxia in an altitude chamber always resulted in partial atrophy of the adrenal glomerular zone and decrease in the synthesis of mineralocorticoids in the adrenals and in their concentration in blood. At the same time, the size of the supraoptic hypothalamic nuclei and their cytogically determined activity diminished. These structurally fixed adaptational changes in the hormonal control caused a stable decrease in the reseves of sodium and water in the organism of the adapted animals. This complex of shifts is contrary to the changes developing in all forms of experimental hypertension and in hypertensive disease in humans. The idea is discussed that inhibition of mineralocorticoid and ACTH secretion and the stable decrease in the sodium and water reserves in the organism during adaptation play the principal role in the mechanism of the preventive effect of adaption to altitude hypoxia in hypertension.
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PMID:[Mechanism of the prophylactic effect of adaptation to altitude hypoxia on the development of hypertension]. 59 30

Interrelations among plasma renin activity (PRA), aldosterone and cortisole levels, 0lood volume, exchangeable sodium, urinary catecholamines, and blood pressure were studied in 35 normal subjects and 60 age-matched non-azotemic patients with diabetes mellitus (60% with hypertension, 15% with orthostatic hypotension). Basal PRA, plasma aldosterone, cortisol, blood volume, plasma potassium, and urinary electrolytes were comparable in diabetic and normal subjects. Diabetic patients, however, had a 10% increase in body sodium (P less than 0.01), and 8% of them showed normal postural PRA responses and subnormal aldosterone responses; 22% had subnormal PRA and normal aldosterone responses, and 17% had subnormal responses of PRA and aldosterone. Non-PRA-related aldosterone responses could not be explained by ACTH or electrolytes. Orthostatic decreases in blood pressure correlated (P less than 0.01) with both catecholamine excretion and basal PRA. This suggests that in diabetes mellitus, body sodium is increased. Basal PRA and plasma aldosterone are usually normal, but their postural responses are frequently impaired. Absent aldosterone responses, despite normal PRA responsiveness, may reflect an adrenal abnormality or an ineffective form of renin. Marked postural aldosterone stimulation, unrelated to PRA, ACTH, or electrolytes, points to a potent unknown factor in aldosterone control. Low levels of free peripheral catecholamines and PRA may be complementary factors contributing to postural hypotension.
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PMID:Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus. 60 91

Virgin and breeder, male and female, Sprague-Dawley rats were unilaterally nephrectomized and given 1% saline drinking water. Animals were injected i.p., twice daily, with a 10 mg/100 g body wt dose of the 11-beta hydroxylation inhibitor, Metyrapone. After 7 weeks of treatment, both the previously nonarteriosclerotic virgin rats and the breeder rats with pre-existing arteriosclerosis developed de nove, widely distributed, intimal hyalinization of their peripheral arteries along with myocardial fibrosis and hyalinization of their intramyocardial coronary arteries. The Metyrapone-treated animals developed severe hypertension with greatly elevated serum creatin phosphokinase, glucose, BUN and cholesterol levels. The adrenal glands, hearts, and kidneys were greatly hypertrophied, in keeping with Metyrapone-induced extra ACTH release and the hypertension-induced myocardial and renal histopathology. Uniparous, Metyrapone-treated, female rats manifested an unusually high incidence of saccular aneurysms of the aorta. It is suggested that the hypertension and the intimal hyalinization and other specific morphologic characteristics of the cardiovascular degenerative changes observed were directly related to excess production of mineralocorticoids, e.g., deoxycorticosterone.
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PMID:Metyrapone-induced cardiovascular degenerative changes in non-arteriosclerotic and arteriosclerotic rats. 63 31

Specific antiserum was raised in white New Zealand rabbits using 18-hydroxydeoxycorticosterone-3-oxime-BSA complex as antigen. The urinary free 18-OH-DOC was estimated after dichloromethane extraction and separation in one paper chromatographic system (propylene glycol/toluene). The mean 18-OH-DOC excretion value (+/- S.D.) in normal subjects was 0.861 +/- 0.527 microgram/24 h (n=23). ACTH produced a 25-fold increase in the excretion of free 18-OH-DOC. Dexamethasone suppressed the values to the lower range of sensitivity. 32% of patients of essential hypertension showed a moderate increase in the free urinary 18-OH-DOC values. The mean value (+/- S.D.) in the low renin hypertension group was 2.50 +/- 1.49 microgram/24 h (n=19), in the normal renin patient group 1.84 +/- 1.22 microgram/24 h (n=38). The difference between controls and the hypertensive groups was statistically significant. Among the different hypertensive groups significant differences could not be calculated.
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PMID:Radioimmunoassay of free urinary 18-hydroxydeoxycorticosterone (18-OH-DOC) in patients with essential hypertension. 65 46

In vitro metabolism of progesterone and cholesterol by the adrenal glands and hepatic delta 4-reductase activity of SHR and ARH were investigated to clarify the possible hyperactivity of the pituitary-adrenal axis and abnormal steroid metabolism in SHR. The increased conversion rate of progesterone to 11 beta-hydroxyprogesterone, corticosterone and 18-hydroxy-deoxycorticosterone and the increased biosynthesis of pregnenolone from cholesterol were noted in ARH, which were similar to those seen with chronic ACTH administration. On the other hand, adrenal steroidogenesis in SHR showed no difference from that of control. Therefore the apparently normal adrenal steroidogenesis in SHR may suggest that the adrenal gland is not involved in the spontaneous hypertension of rats. The markedly decreased hepatic delta 4-reductase activity in ARH and SHR was observed in this investigation.
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PMID:Adrenal steroidogenesis and hepatic corticosteroid metabolism in hypertensive rats. 66 27

A unique syndrome in a three-year-old American Indian girl was characterized by signs and symptoms of mineralocorticoid excess in the absence of excessive secretion of any known sodium-retaining steroids. Hypertension and hypokalemic alkalosis were corrected by spironolactone or a low sodium diet. Plasma renin activity was suppressed but the secretion of aldosterone was undetectable and was not stimulated by salt depletion. There was no evidence of abnormal accumulation of aldosterone precursors and metabolism of a tracer dose of the hormone was normal. Secretion rates of cortisol, corticosterone, deoxycorticosterone, deoxycortisol and aldosterone were very low and did not increase normally with ACTH administration. However ACTH administration aggravated hypertension and hypokalemia. Dexamethasone did not improve hypertension. Despite low secretion of glucocorticoids and mineralocorticoids, the patient showed no addisonian features and survived severe illness. Secretion of a factor of adrenocortical origin was suggested by the exacerbation of the syndrome of ACTH. The unidentified factor appears to be both a potent glucocorticoid and mineralocorticoid.
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PMID:Evidence for an unidentified steroid in a child with apparent mineralocorticoid hypertension. 87 May 17

Hypertension and hypokalemia occur in patients with Cushing's syndrome whereas aldosterone production is normal and plasma renin activity is usually normal or increased. A normal aldosterone level in the face of suppressed plasma renin activity is unusual and suggests excess mineralocorticoid hormone activity. Our patient, who had Cushing's syndrome due to adrenocortical adenoma, can be classified as having low renin hypertension (suppressed renin and normal aldosterone levels). The mineralocorticoid hormone in excess was deoxycorticosterone which suppressed renin. The aldosterone production was normal and was produced solely by the adenoma. Contralateral adrenal gland suppression of both the zona glomerulosa by deoxycorticosterone via renin, and of the fasciculata by cortisol via ACTH was demonstrated after removal of the adenoma. Normal adrenal function was gradually restored.
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PMID:Concurrent hypercortisolism and hypermineralocorticoidism. 87 Nov 29

In 16 patients with hypokalemic hypertension the combination of abnormally high and unsuppressible plasma aldosterone with low or undetectable renin activity led to the diagnosis of primary aldosteronism. To differentiate between aldosterone producing adenoma and idiopathic bilateral hyperplasia, determination of aldosterone concentration in both adrenal veins was performed in 12 patients. In 4 of these patients the two forms of primary aldosteronism could not be differentiated as in these cases only one of the two adrenal veins simultaneously showing an abnormally high aldosterone concentration could be canulated. Plasma aldosterone and plasma cortisol were determined overnight (20.00-8.00 h) at short time intervals in 8 patients with adenoma, 1 patient with carcinoma of the adrenal cortex and 3 patients with bilateral hyperplasis. In all patients with adenoma a significant correlation between aldosterone and cortisol was observed (p less than 0.05-0.001) whereas no correlation was seen in the patients with hyperplasia and carcinoma. The clinical importance of these findings is that in the presence of ACTH-dependent secretion of aldosterone the site of the adenoma can be predicted even when blood from only one adrenal vein is obtained.
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PMID:[Primary aldosteronism: diagnosis, laterality and regulation of hormone secretion]. 121 58

The radioimmunological dosages of renin and of aldosterone are used nowadays in clinical practice for research purposes only. The measurement of activity of plasma renin may be considered a significant indication of the concentration of the enzime in plasma and, indirectly, of its secretion. Several factors take a part in the regulation of renin secretion (mean arterial pressure, introduction of sodium and potassium, the sympathetic nervous system, ADH and concentration of angiotensin II in plasma). In pathological conditions such factors may cause alteration of the renin-angiotensin II system, thus determining hyperreninisms and hyporeninisms, whether associated with arterial hypertension or not. Several factors take a part on aldosterone secretion too (ACTH, sodiaemia, potassiaemia, renin-angiotensin II system). In pathological conditions the alteration of the regulation system may lead to hyperaldosteronism or to hypoaldosteronism of primary or secondary type. A survey of recent research on the physiopathology of the renin-aldosterone system is also given.
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PMID:[Renin and aldosterone]. 123 75

The syndrome of primary aldosteronism is caused either by an aldosterone-producing adenoma or by idiopathic bilateral adrenal hyperplasia. Hypokalemic hypertension is the leading symptome of the disease. Diagnosis is by the combination of abnormally high and non-suppressible aldosterone values with undetectable or low renin values unresponsive to postural changes or salt restriction. Patients with aldosterone-producing adenoma normally show a fall in plasma aldosterone in response to posture and ACTH-dependent circadian rhythm of aldosterone, whereas bilateral hyperplasia is characterized by postural increases in plasma aldosterone and an ACTH-independent diurnal aldosterone rhythm. These creteria serve to differentiate between adenoma and hyperplasia. An aldosterone-producing adenoma can be localized by veinography, determination of aldosterone concentration in both adrenal veins and by 131I-cholesterol scintigraphy. In our hands the determination of aldosterone in blood from both adrenal veins is the most efficient procedure. In interpreting the results, however, rhythmic and sudden changes in adrenal hormone secretion should be considered. In cases where no adrenal venous blood is obtained, 131I-cholesterol scintigraphy may be used to localize adenoma. In patients with aldosterone-producing adenomas unilateral adrenalectomy should be performed, whereas patients with idiopathic bilateral hyperplasia should receive antihypertensive therapy. As rare instances of primary aldosteronism, a case of aldosterone-producing carcinoma of the adrenal cortex and a case of presumably unilateral adrenal hyperplasia are reported.
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PMID:[Primary aldosteronism]. 126 63


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