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

The relative contribution of the renin-angiotensin system, adenocorticotrophic hormone (ACTH) and plasma electrolytes in the response of plasma aldosterone to 30 minutes of 65 degrees head-up tilt was assessed in 10 essential hypertensive patients. Studies were carried out before and during acute blockade of renin release by propranolol, ACTH suppression by dexamethasone and combined renin and ACTH blockade. In control studies orthostasis induced significant increases only in plasma renin activity and aldosterone. In contrast, when the renin response to tilt was acutely suppressed by propranolol administration, the aldosterone response was nonetheless maintained but now appeared to be under ACTH control, since concurrent increases in cortisol were observed. During ACTH suppression aldosterone increased during tilt and so did renin. However, during combined ACTH and renin blockade aldosterone failed to increase during tilt. These studies suggest that the aldosterone secretory response to head-up tilt is normally mediated by the renin-angiotensin system but, when the renin response is suppressed, an ACTH response is elicited which assumes a backup role. However, when these two systems are blocked other factors appear unable to respond during tilt to support a normal aldosterone response.
Hypertension
PMID:The substitutive role of ACTH in supporting aldosterone response to head-up tilt during acute renin suppression in patients with essential hypertension. 4 68

A 24-year-old woman was referred to our clinic because of severe hypocalemic hypertension and latent myocardial insufficiency. Plasma renin activity and plasma aldosterone concentration were lowered. Plasma cortisol concentrations and the urinary excretion of vanillin mandelic acid were found within normal range. Some efforts to identify a specific adrenal enzymatic defect were unsuccessful. By combined therapy with spironolactone, methyldopa and clonidine, the blood pressure was significantly lowered, but not normalized. Triamterene had also an expressed hypotensive effect and induced orthostatic phenomena. After six months of hypotensive drug therapy, the patient's mother reported that her daughter consumed for more than seven years high doses of special nasal drops containing, beside ephedrine and naphazoline, the potent mineralocorticoid 9-alpha-fluoroprednisolone. A strong drug-dependence to the naphazoline component could be evaluated. The application of the mineralocorticoid was stopped, and only a slight low-sodium diet had to be added to restore the long-standing elevated blood pressure to normal
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PMID:Severe arterial hypertension caused by chronical abuse of a topical mineralocorticoid. 5 37

Hypertension was found in four patients after unilateral renal-artery thrombosis following blunt abdominal trauma. In one patient, who was followed up from the time of injury, renin hypersecretion and secondary aldosteronism developed within a few days, and hypertension was present 12 weeks later. Increasing haemoglobin and raised blood-erythropoietin concentrations were also found. In the three other patients, hypertension was found casually within 3 years of trauma. In all patients, unilateral renin production by the affected kidney was significantly increased. Nephrectomy of the diseased kidney corrected hypertension and endocrine abnormalities in all patients. The delayed onset of hypertension despite early activation of the renin/angiotensin/aldosterone axis accords with the course of events observed in experimentally induced hypertension in rats, and suggests that several weeks or even months are required for hypertension to develop after sudden renal-artery occlusion in man. Slowly acting mechanisms, probably initiated by hypersecretion of renin, may be responsible for the hypertension.
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PMID:Renin/angiotensin system in hypertension after traumatic renal-artery thrombosis. 5 38

In two hypertensive patients with renal-artery stenosis, overactivity of the renin-angiotensin system was ruled out by investigations of renin and aldosterone concentrations and by the lack of a vasodepressor response to angiotensin blockade with saralasin. Nevertheless, hypertension was cured by renal revascularisation. The date suggest that there is a form of renovascular hypertension which is not mediated by the renin-angiotensin system.
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PMID:Non-renin-mediated renovascular hypertension: A new syndrome? 6 24

Pronounced hypoaldosteronism was found in three young women with hypertension and symptoms of mineralocorticoid overproduction--i.e., hyporeninaemia, hypokalaemia, and a fall in blood-pressure after diuretic therapy. Plasma 11-deoxycorticosterone and 18-hydroxy-11-dooxycorticosterone concentrations were normal Treatment with dexamethasone induced a return to normal of blood-pressure and plasma-potassium and an increase in plasma-renin activity and urinary aldosterone excretion. The data suggest that hypertension in these patients is maintained by overproduction of an unknown adrenocorticotropindependent mineralocortocoid.
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PMID:Dexamethasone-responsive hypertension in young women with suppressed renin and aldosterone. 7 49

A 57-year-old woman with hypertension and moderate renal insufficiency had chronic unexplained hyperkalaemia. Metabolic balance studies confirmed a diagnosis of hyporeninaemic hypoaldosteronism. Two observations suggested that impaired renal prostaglandin production contributed to the pathogenesis of the patient's disorder. Baseline renal-prostaglandin synthesis (as determined by urinary excretion of P.G.E and P.G.F) was was substantially depressed when compared with that in nine normal females. Infusion of low doses of P.G.A1 produced a significant increase in serum-aldosterone and urinary potassium excretion; it also led to a dramatic fall in blood-pressure and serum-potassium. It appears from these studies that a defect in renal prostaglandin synthesis has an important role in the pathogenesis of hyporeninaemic hypoaldosteronism.
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PMID:Possible role for impaired renal prostaglandin production in pathogenesis of hyporeninaemic hypoaldosteronism. 8 82

The renal abnormality which causes hypertension in the Milan hypertensive strain of rats disappears as hypertension develops. Because of the many analogies between the condition in these rats and "essential" hypertension in man, the same pattern of change may occur if a renal abnormality is the cause of essential hypertension in man. This hypothesis was tested in two groups of young normotensive subjects matched for age, sex, and body-surface area; in the first group both parents were hypertensive, and in the second group both parents were normotensive. Renal plasma-flow, glomerular filtration-rate, plasma-volume, plasma-renin activity, plasma-concentrations of Na+, K+, and catecholamines, 24 h urinary excretion of Na+, K+, and aldosterone, and the cardiac index were measured so that renal function and the role of factors affecting blood-pressure regulation could be assessed. Renal plasma-flow was significantly higher (p less than 0.01) in the first group, whereas results of tests for all the other factors were almost the same in both groups. The hypothesis that a primary kidney abnormality causes hypertension in a proportion of patients with essential hypertension is proposed.
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PMID:A renal abnormality as a possible cause of "essential" hypertension. 8 3

11 patients with primary aldosteronism have been encountered over 11 years and submitted to surgery in a provincial teaching hospital serving a population of 3 million. Contrary to classical teaching, the hypertension has usually been very severe. Precise identification of the site of the lesion preoperatively has been possible by the measurement of adrenal-vein aldosterone levels, and results of surgery have been excellent. The iodocholesterol adrenal scan also correctly identified the site of the adenoma in 5 out of 7 patients in which it was used. Adrenal venography was of little value except in siting catheters.
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PMID:Severe hypertension in primary aldosteronism and good response to surgery. 8 65

16beta-Hydroxydehydroepiandrosterone (16beta-OH-DHEA) and related C19-steroids have recently been reported to be etiologic in low-renin essential hypertension. The mineralocorticoid potency of 16beta-OH-DHEA and several C19-steroids (16-oxo-A-diol, 16-oxo-testosterone, 16beta-OH-epiandrosterone, 5-androstene-3beta, 16beta,17beta-triol, 19beta-OH-testosterone, 18-OH-DHEA, and 16alpha-OH-DHEA) were investigated in two different rat bioassay systems under a variety of experimental conditions. In all but one instance, only negligible mineralocorticoid activity was observed, usually less than 0.1 per cent that of aldosterone. Since 16beta-OH-DHEA has negligible mineralocorticoid activity in the rat bioassay and the toad bladder assay (as reported by others), does not cause hypertension when injected chronically into the rat, and does not displace aldosterone from its renal receptors, it appears unlikely to be etiologic in low-renin essential hypertension. On the other hand, when 16-oxo-testosterone was injected intraperitoneally instead of subcutaneously, it demonstrated a slight increase in mineralocorticoid activity (from less than 0.1 per cent to 0.2 per cent) which equaled that of 18-hydroxydeoxycorticosterone (18-OH-DOC) injected subcutaneously. Thus, the possibility remains that 16-oxo-testosterone or a closely related metabolite may have sufficient mineralocorticoid activity to be involved in certain forms of hypertension in man.
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PMID:Mineralocorticoid activity of 16beta-hydroxydehydroepiandrosterone and related steroids. 13 37

A previously unidentified mineralocorticoid, 16beta-hydroxydehydroepiandrosterone (16beta OH-DHEA) has recently been isolated from urine extracts of patients with low-renin hypertension and reported to possess one-fortieth the mineralocorticoid potency of aldosterone by bioassay. However, using a radioreceptor assay, we demonstrate the affinity of 16beta-OH-DHEA for renal 3H-aldosterone receptors to be only 0.011 per cent that of unlabeled aldosterone. 16beta-OH-DHEA therefore would not be expected to possess significant mineralocorticoid properties unless its mechanism of action involves binding to a unique class of renal receptors. Until these discrepancies between bioassayable mineralocorticoid activity and affinity for mineralocorticoid receptors can be resolved, the role of 16beta-OH-DHEA in the pathogenesis of low-renin hypertension remains speculative.
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PMID:Interaction of 16beta-hydroxydehydroepiandrosterone with renal mineralocorticoid receptors. 13 38


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