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

The Authors examine the antihypertensive effectiveness of the beta-adrenergic receptor blocking agents, according to their personal experience and a review of the bibliography. It is not cleared yet how these drugs reach their hypotensive effect. It is reasonable to assume however that several factors are involved: cardiac output, intravascular volume changes, plasma renin activity and peripheral resistance. Thirty patients suffering from essential hypertension not complicated by cardiac or renale failure were treated. Patients were allocated at random into one of three subsets of ten. In group A oxprenolol was given for 8 weeks and the dose was gradually increased up to 300 mgs daily. Oxprenolol was administered in combination with clortalidone in group B and with phentolamine in group C. A clinically satisfactory reduction in blood pressure was attained in no subset, despite the significant decrease of mean blood pressure. The blockade of beta-adrenergic receptors alone has proved to be less effective than the combined administration of oxprenolol and clortalidone or of oxprenolol and phentolamine. No differences were observed between the two combinations.
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PMID:[Beta-blocking agents alone or combined with diuretics or alpha-adrenolytics in the treatment of essential arterial hypertension]. 4 88

Ten patients affected by essential moderate or severe hypertension were given five sequential treatments, each for three weeks: 1) placebo, 2) chlorthalidone (Cl) 100 mg daily, 3) Cl 50 mg + oxprenolol slow release (Ox) 160 mg daily, 4) Ox 160 mg and 5) Ox 320 mg daily. Four subjects poor responders (DPB greater than or equal to 110 mmHg) received a later administration of Ox 160 + Cl 50 + hydrallazine (Hydr) 25-100 mg daily. Both groups of patients showed the greatest antihypertensive action with Ox 160 + Cl 50 mg daily. Oxprenolol induced a similar hypotensive effectiveness at 160, as well as 320 mg/day. Relationship between plasma renin activity (PRA) values and antihypertensive response to each treatment takes the following conclusions: 1) Basal PRA levels cannot be a guide for preferential choice of diuretic or betablocking therapy. 2) It is likely that renin activated by Cl and Hydr partially blunts their hypotensive activity. On the contrary, essential hypertension with normal or low PRA does not seem depending on angiogensinogenic factors. 3) Oxprenolol remarkably inhibits the overreninism induced by chlorthalidone and hydrallazine, in such way increasing their antihypertensive action. 4) In the management of essential moderate or severe hypertension is preferable to employ a mild dosage of betablockers and diuretics, rather than use higher doses of a single agent.
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PMID:[The role of renin after betablocking diuretic and vasodilator treatment in essential hypertension (author's transl)]. 4 15

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

Serum-potassium and total body potassium (T.B.K.) were measured serially for 1 year in a group of eighteen patients with mild essential hypertension. The patients were receiving a single daily dose of 10 mg. bendrofluazide without potassium supplements. At 12 months the mean value for serum-potassium (3-86 mmol per litre) was significantly lower than the mean pre-treatment value (4-26 mmol per litre). There was no significant decrease in T.B.K. in the same period. Diastolic blood-pressure fell significantly, and there were no apparent side-effects from the medication. In the group as a whole, a reduction of about 1 mmol per litre in serum-potassium was associated with an average reduction of 10% in T.B.K., but there was a large individual variation. The amount of potassium loss during the period of study did not seem to be clinically significant. It is suggested that routine potassium supplements are not essential in the treatment of uncomplicated essential hypertension with thiazide diuretics.
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PMID:Total body and serum potassium during prolonged thiazide therapy for essential hypertension. 4 97

Severe essential hypertension in a subset of American black subjects is associated with marked stenosis of interlobular arteries and arterioles of the kidneys, observed by renal biopsy and binephrectomy specimens. The interlobular arterial stenosis is caused by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material, and acid mucopolysaccharide. Because of this makeup, we propose the term "musculo-mucoid intimal hyperplasia" for this lesion. The media of these arteries appears maximally dilated, and by electron microscope displays degenerative changes of the smooth muscle cells. The arterioles are thickened, due mainly to hyalinization, but also due to the musculo-mucoid change (onionskin effect). The smooth muscle cells are degenerated and atrophic. These patients do not exhibit fibrinoid necrosis of the arteries, arterioles, and glomeruli, presumably because of the rapidity of the development of the arterial stenotic lesion. Accordingly, the glomeruli are destroyed by ischemia, and there is no evidence of glomerulitis (no "Kombinations" form of Fahr). A unifying hypothesis concerning renal hypertensive arterial disease is suggested by these studies. This hypothesis places the main emphasis for all the morphological expressions of the intrinsic visceral vasculature on changes involving the main functional unit of the vessel wall, the medical smooth muscle.
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PMID:Malignant hypertension due to musculo-mucoid intimal hyperplasia of intrarenal arteries. Absence of renal fibrinoid necrosis. 4 31

Cation transport and electrolyte composition were studied in leucocytes from 17 patients with uncomplicated essential hypertension. Significant increases in cell sodium and water contents, associated with a depression of the rate-constant for active sodium efflux, were found in the hypertensive patients. These abnormalities in cell sodium transport may possibly be related to mechanisms of hypertension.
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PMID:Abnormal leucocyte composition and sodium transport in essential hypertension. 4 73

In a random sample of normotensive and hypertensive fifty-year-old men plasma-renin-activity (P.R.A.), plasma-renin-concentration (P.R.C.), and renin substrate were measured using radioimmunoassay for angiotensin I. P.R.A. in normotensives and untreated hypertensives were normally distributed with slight skewness to the right. The mean P.R.A. for untreated hypertensives (0.65 ng. per ml. per hour) was slightly, but not significantly, lower than that of the normotensive reference group (0.78 ng. per ml. per hour). Previously untreated hypertensives who had been off treatment for four weeks had either high or low P.R.A. depending on the previous treatment. No differences in the angiotensin-generation rate were noted as judged from the P.R.A./P.R.C. ratio. No differences in the renin-substrate concentration between the groups were found. The findings suggest that renin changes in essential hypertenion are secondary to pressure changes. Thus, the renin-angiotensin system may not be of primary pathogenetic importance in the development of essential hypertension.
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PMID:Renin-angiotensin system in essential hypertension. 5 Nov 45

It is proposed that essential hypertension is an exaggeration of the tendency for blood-pressure to rise with age, that it results from a repeated sequence in which a small rise in pressure, possibly resulting from an autonomic nervous overactivity, produces changes in the kidney which maintain the rise of pressure and become the basis for a further rise.
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PMID:Pathogenesis of essential hypertension. 5 62

Study of general haemodynamics in 15 patients with low-renin essential hypertension showed haemodynamic and pathophysiological heterogeneity. However, there was suppression of sympathetic nervous system function in all low-renin patients, regardless of haemodynamic pattern. Subnormal sympathetic nervous activity was manifested by a low normal mean plasma-noradrenaline concentration at rest, diminished noradrenaline responsiveness to postural stimulation, and a reduced blood-pressure response to the indirectly acting sympathomimetic amine tyramine. It is proposed that the syndrome of low-renin essential hypertension is of diverse aetiology, but with secondary sympathetic nervous system underactivity as a feature common to the various forms. The low plasma-renin activity is probably an expression of defective sympathetic nervous system stimulation of renin release.
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PMID:Suppression of sympathetic nervous function in low-renin essential hypertension. 5 83


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