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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 substantial group of patients with essential hypertension have abnormally low renin levels which respond poorly to stimulation. Important differences in response to therapy and in prognosis have been described between these and other hypertensive patients. It is suggested that the vascular changes of nephrosclerosis, which may be seen in both hypertensive and normal subjects, result in a reduction of afferent arteriolar distensibility, with impairment of basal renin secretion and responsiveness. This hypothesis accords with both of the known clinical characteristics of low-renin hypertension and with the known effect of arterial changes upon the activity of other baroreceptors.
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PMID:Low-renin hypertension: nephrosclerosis? 4 26

A study of the frequency distribution of plasma-renin concentration in 81 patients with essential hypertension produced no evidence of a distinct sub-population with low renin levels. An arbitrary dividing line was used, therefore, to define low-renin hypertension (36% of patinets). Patients in this group were older than those with normal renin levels, and there was a significant negative correlation between renin and age among all patients. Low-renin hypertension was not characterized by increased exchangeable sodium, but exchaneable postassium was significantly lower than in patients with normal plasma-renin. This difference became insignificant when five patients in the low-renin group with persistent hypokalaemia were excluded. It is concluded that low-renin hypertension does not represent a separate diagnostic entity but that plasma-renin falls with age in essential hypertension.
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PMID:Is low-renin hypertension a stage in the development of essential hypertension or a diagnostic entity? 4 18

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

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.
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PMID:Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats? 5 84

The proportion of cases of hypertension with a renal cause which can be corrected by surgery is very small. Radiological diagnosis of such a cause is expensive and time-consuming; hence the rewards of intensive investigation are small compared with the cost. Measurement of plasma-renin offers a good method of selecting those patients who require further investigation, if the cut-off point is carefully considered in the light of the acceptable incidence of false-positive and false-negative results.
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PMID:The hunt for renal hypertension. 5 49

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

The effect of infusion of the angiotensin II antagonist P113 on blood-pressure (B.P.) has been studied in 10 patients with various forms of hypertension under four different conditions: before and after salt depletion and with or without propranolol treatment. The fall in B.P. after P113 infusion significantly correlated with log P.R.A. (plasma-renin activity), irrespective of diagnosis or treatment. P113 infusion caused a consistent fall in B.P. only after sodium depletion. The changes in B.P. after P113 infusion and those induced by propranolol correlated only during sodium depletion, when P.R.A. values rose. It is concluded that sodium depletion induced "renin dependency" of B.P. in all patients. The decrease in B.P. renin dependency after propranolol therapy suggests that suppression of P.R.A. is one of the antihypertensive mechanisms underlying the action of this drug.
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PMID:Renin dependency of blood-pressure. Analysis by angiotensin II antagonist P113 in hypertensive patients treated with salt depletion and propranolol. 5 53

The effect of propranolol has been studied in two patients with chronic renal failure and hypertension which remained refractory despite the removal of excess sodium and water by dialysis. Measurements of plasma-renin, exchangeable sodium, and blood-volume demonstrated that in both patients hypertension was due to excess renin. The administration of propranolol was followed by a rapid fall in blood-pressure to normal, thereby obviating the need for bilateral nephrectomy. In both patients the fall in blood-pressure was accompanied by a striking fall in plasma-renin, and in one there was a highly significant association between plasma-renin activity and mean arterial pressure.
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PMID:Effect of beta-adrenergic blockade on plasma-renin activity and intractable hypertension in patients receiving regular dialysis treatment. 5 51

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


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