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

Accumulating evidence suggests that the central nervous system plays a fundamental role in chronic hypertension. On the other hand, the means by which nervous factors influence the long-term control of blood pressure remain obscure. Animal models that replicate some of the functional aspects of essential hypertension in man have been of value and continue to provide insight into the complexity of the problem. Although none of the experimental models gives definitive answers, separate and combined analyses suggest the multiplicity of sites at which the stimulus must be applied for blood pressure to remain elevated.
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PMID:Animal models, hypertension, and central nervous system mechanisms. 32 2

This study was designed to compare the effectiveness of spironolactone, hydrochlorothiazide, and combined spironolactone-hydrochlorothiazide therapy in patients with low renin and those with normal renin essential hypertension. Patients with low renin hypertension had a greater hypotensive response to each regimen (p less than 0.001). Low renin patients responded equally to both spironolactone and to hydrochlorothiazide, and in low renin but not in normal renin patients reduction of blood pressure correlated with weight loss. These results suggest that a volume factor, not specifically related to increased mineralocorticoid production, contributes to the pathogenesis of low renin essential hypertension.
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PMID:Diuretic therapies in low renin and normal renin essential hypertension. 32 59

Saralasin, a specific competitive inhibitor of angiotensin II, was administered in a controlled, prospective study designed to test the hypothesis that this agent is a useful tool for the detection of renovascular hypertension. 13 patients, 11 with renovascular hypertension and 2 with high-renin essential hypertension, showed a gross, readily apparent decrease in blood pressure after receiving saralasin. 8 patients with essential hypertension and normal or low renin levels exhibited no depressor response to the drug. In the patients with renovascular hypertension, blood pressure response during angiotensin blockade compared favourably with renal vein renin determinations as a predictor of operative results. Because saralasin testing has resulted in few if any falsely positive or negative results when considered as a diagnostic procedure for renin-mediated hypertension, and because it is safe, it may become an ideal initial screening procedure. The saralasin test (either bolus injection or sustained infusion) is completely valid only if the patient is mildly salt-depleted, is not taking other antihypertensive medication, and is genuinely hypertensive at the time of the test.
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PMID:Angiotensin blockade in renovascular hypertension: a controlled, prospective study. 33 16

Renin-aldosterone profiling was used to classify patients with hypertension: 243 patients with essential hypertension were classified by renin-urinary sodium indexing; 107 were reclassified by response to administration of furosemide and intravenous saline; 45 were further classified by response to a low-sodium diet. Arbitrary "normal ranges" were determined in 89, 32, and 38 volunteers, respectively. Patients with low-renin apparently do not have "high-volume" hypertension. Rather, they show a primary renal abnormality in renin secretion and become relatively deficient in angiotensin II and aldosterone when they are subjected to diuresis. They can maintain aldosterone secretion under normal conditions because their adrenal aldosterone receptor is supersensitive to angiotensin II. No evidence of abnormal sympathetic neural activity was found among the renin subgroups. Renin-aldosterone profiling in current clinical practice seems useful mainly in the detection of patients with curable forms of secondary hypertension. Aldosterone/renin ratios may be particularly helpful in diagnosis when obtained after a patient has undergone expansion or contraction of his extracellular fluid volume.
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PMID:Renin-aldosterone profiling in hypertension. 33 42

Acebutolol, a new cardioselective beta-adrenoceptor blocking agent, has been evaluated for the treatment of hypertension. Thirty eight previously untreated male patients with essential hypertension received placebo treatment during a 4-week run-in period, and then they were randomly (double-bind) allocated either to continued placebo treatment for three 4-week periods or to treatment with acebutolol 400, 600, and 1200 mg daily, respectively, for three 4-week periods. Blood pressure and heart rate were recorded at the end of each 4-week period. Treatment with acebutolol produced statistically significant reductions in blood pressure and heart rate as compared to the placebo regimen.
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PMID:Controlled trial of acebutolol in hypertension. 33 78

Two-months' administration of 2.5 mg/day indapamide, preceded and followed by 2 weeks of a placebo, led to a significant fall in pressure values and normalisation of diastolic pressure in a high percentage of 47 subjects, mostly with essential hypertension, in a controlled multi-centre trial. Absence of toxic effects, tolerance and therapeutic activity at low doses recommend the drug for most cases of arterial hypertension.
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PMID:[Controlled multicentric trial of the antihypertensive agent indapamide]. 33 32

A double-blind, crossover, multicentre study of 98 previously untreated patients with mild to moderate essential hypertension was carried out in general practice to assess the effect of 50 mg, 100 mg, and 200 mg atenolol, given once daily, compared with that of placebo over a period of 4 weeks each. At the end of the double-blind phase, all patients took 100 mg atenolol daily for a further 8 weeks. All three doses of atenolol produced statistically significant falls in systolic and diastolic pressure and pulse rate (p less than 0.001). The lowest pressures were achieved with 100 mg daily; a difference of 22/15 mmHg at the end of the double-bling phase, and a difference of 25/16 mmHg at the final observation. Body weight, blood urea, blood uric acid, and serum electrolytes remained within normal limits throughout the study. The incidence of side-effects with 50 mg and 100 mg atenolol was not significantly different from that caused by placebo, but the incidence of tiredness at the 200 mg dose level was greater than that caused by placebo and by the lower doses. The incidence of possible side-effects elicited by a questionnaire was low, the greatest number being volunteered by patients taking placebo. It is concluded that the optimal dose of atenolol for treating patients with mild to moderate hypertension in general practice is 100 mg daily.
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PMID:A dose-response study of atenolol in mild to moderate hypertension in general practice. 34 Jan 36

Our clinical experience and the literature regarding anesthetic management of the hypertensive patient are reviewed. Preoperative evaluation and treatment of all hypertensive patients, regardless of their degree of lability, is recommended. For emergency surgery on an untreated hypertensive patient, control of blood pressure with nitroprusside should be attempted before an awake or rapid sequence intubation. The evaluation of hypertension, the physiology of idiopathic hypertension, and the effects of treatment are discussed.
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PMID:Hypertension and anesthesia: cause for concern. 34 39

The hypertensive preparation "Tendor" of the Hungarian firm "Chinoin" was applied in the treatment at the Clinic of Propaedeutics of Internal Diseases. For the period from 1975-1977, 28 hospital patients and 8 out-patient department department patients with essential hypertension were followed up. Especially good effect was obtained among the patients in II and II stage with light and moderate hypertension degree among the group followed up. The favourable effect of the preparation is manifested as early as the first 10-12 days after treatment, without the combination of "Tendor" with some other hypotensive remedies.
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PMID:[Treatment of hypertension with the preparation Tendor]. 34 31

After 30 years of continuous research into the mechanisms of human hypertension, we summarize the results obtained by the members of the multidisciplinary research group on hypertension of the Clinical Research Institute of Montreal on the disturbances of minerlocorticoid activity in a rigorously selected group of patients with early, mild essential hypertension. We attempt to integrate these findings with those of many other groups working on other aspects of hypertensive cardiovascular diseases. On the assumption that the increased peripheral resistance responsible for hypertension results from an imbalance or a disturbance of the equilibrium between the sympathetic nervous system and norepinephrine on one hand, and the vascular tone, sensitivity and responsiveness of the arterial smooth muscle to norepinephrine and to angiotensin II on the other hand, three models that fit the experimental and clinical facts as known at present are described.
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PMID:Role of the adrenal cortex and sodium in the pathogenesis of human hypertension. 34 5


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