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

Measurement of the blood volume in cases of essential hypertension has shown a negative correlation with increase in blood pressure. We have been able to distinguish a group of moderate hypertensives who are hypervolemic, and whose systemic effect is more marked than in the moderate hypovolemic type. Such cases respond poorly to single drug therapy with beta blockers, but well to diuretics. The authors propose a general treatment scheme for essential hypertension: single therapy (beta blockers or diuretics) in mild cases of hypertension; single therapy by diuretics in the moderate types with the increased volume; single therapy by beta blockers in the moderate types with low volume, multiple treatment with the drugs together in cases of severe hypertension.
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PMID:[Importance of measuring blood volume by an isotope method in essential hypertension]. 3 Apr 25

Recent research shows that the renin-angiotensin-aldosterone axis either maintains or causes some or all of the high blood pressure of most patients and demonstrates anew that renin-sodium profiling defines this involvement. Performed with a serum potassium measurement, this now reliable test is useful for primary screening and then, in conjunction with renal vein renin studies or an aldosterone profile, for diagnosis or exclusion of surgically curable renovascular or adrenocortical hypertensions. For the remaining majority with essential hypertension, renin profiling exposes the relative participation of either vasoconstriction or volume factors, thereby guiding simpler, more specific, and predictably effective antirenin or antivolume treatments. Renin profiling identifies those in whom treatment should begin with a beta-blocker as opposed to a diuretic while not infrequently also providing baseline information about severity and prognosis in individual patients.
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PMID:Renin profiling for diagnosis and treatment of hypertension. 3 92

1. Active and acid-activable inactive renin were measured in renal venous and arterial plasma of 18 patients with essential hypertension (EHT) and 19 patients with renovascular hypertension (RVHT). In seven patients with EHT and in 11 patients with RVHT measurements were made before and 25-35 min after an intravenous injection of 300 mg of diazoxide. 2. Under basal conditions the renal vein to artery ratios for active and inactive renin in EHT ranged from 0.71 to 1.96 and from 0.68 to 1.44 respectively. In 14 patients with RVHT the renal vein to artery ratio for active renin on the affected side was above the range found in EHT and in six of them the renal vein to artery ratio for inactive renin was also elevated. 3. The diazoxide-induced release of active renin from kidneys, which had a stenotic artery but were not seriously contracted, was associated with a fall of the renal vein to artery ratio for inactive renin to a value below 1.00. 4. The results indicate that changes in the release of active and inactive renin do not always run in parallel. The findings are compatible with the hypothesis that circulating inactive renin can be activated in the kidney.
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PMID:Renal release of active and inactive renin in essential and renovascular hypertension. 3 2

Nadolol, a new beta-adrenergic blocking agent, was administered orally in gradually increasing single daily doses to 13 hospitalized patients with essential hypertension. Maximal doses ranged from 200 to 480 mg/day. Blood pressure was reduced in nine patients and heart rate was decreased in 11 patients. The decrease in blood pressure was either partial or temporary in five of the nine patients who responded. Concomitant administration of the diuretic chlorthalidone decreased blood pressure in a previously unresponsive patient. Nadolol effectively inhibited isoproterenol-induced tachycardia and decreased cardiac output by 18 per cent. Plasma renin activity and plasma aldosterone concentration were not changed significantly by the treatment. Body weight was not altered significantly. Blood pressure response was independent of the pretreatment renin levels or the change in renin induced by nadolol; it was also independent of the changes in cardiac output and heart rate but was more pronounced in patients with milder baseline hypertension. The decline in serum concentration of nadolol was consistent with the drug's reported half-life of 12.2 hours. The results indicate that single daily doses of nadolol alone can reduce blood pressure significantly with minimal cardiodepressant effects and no important side effects. The effectiveness of nadolol may be enhanced by the addition of a diuretic.
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PMID:Effect of nadolol in treatment of hypertension. 3 98

1 Echocardiography showed 14 of 24 patients with essential hypertension to have hypertrophy of their left ventricular walls. In eight of these 14 patients the left ventricular configuration initially fulfilled the criteria for asymmetric septal hypertrophy (ASH) and six were symmetrically hypertrophied, the remaining ten being normal. 2 Following 12 weeks' treatment of hypertension with the object of reducing the supine BP to 150/90 mmHg or below, there was a reduction of wall thickness so that only two of the eight continued to show ASH. 3 The six patients with symmetrical left ventricular hypertrophy also showed a significant reduction in the thickness of the septum and the posterior wall. Those with normal echocardiograms did not change. 4 This reduction of wall thickness produced by antihypertensive therapy may represent regression of left ventricular hypertrophy.
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PMID:Regression of left ventricular hypertrophy during treatment with antihypertensive agents. 3 79

The setting generality of treatment effects was examined for a client with 3 years' history of essential hypertension. Self-control progressive relaxation training led to durable normotensive blood pressures (BP) in the natural environment and psychology clinic, although medical setting BP remained elevated. Further assessment indicated that this latter problem was a function of conditioned anxiety to medical setting stimuli. Systematic desensitization led to reductions in medical setting BP to normotensive levels, and laboratory psychophysiological assessments confirmed the elimination of the anxiety response. The present case study raises the issue of to what extent such reactive hypertension is a problem for other individuals similarly diagnosed and demonstrates the importance of the assessment of generality of treatment effects for essential hypertension.
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PMID:Setting generality of blood pressure reductions and the psychological treatment of reactive hypertension. 4 35

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

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


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