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

The antihypertensive activity of timolol (Blocadren, FROSST-MSD), a new beta blocking agent, was assessed in a single blind crossover placebo-controlled study in 14 patients with essential hypertension. Ten patients completed the trial. The average standing pressure during the placebos periods was 168/109mmHg and during the periods on treatment with timolol the average standing pressure was 139/92mmHg. All 10 patients showed some hypotensive response. The average daily dosage was 21 mg with a range of 15-30 mg. Four patients achieved optimal levels of blood pressure by the end of one week's therapy with the maximum time required being four weeks. Timolol appears to be an effective antihypertensive agent. Side effects were insignificant.
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PMID:Timolol maleate (Blocadren) in the treatment of essential hypertension. 0 95

Commercially available columns for ion exchange chromatography were used for the separation of catecholamines in urine. The estimation of catecholamines was performed fluorimetrically by a new trihydroxyindole method. The fluorescence of adrenaline or noradrenaline was enhanced, in comparison with other methods, by the combined application of boric acid, copper-ions, mercaptoethanol and final reacidification. The fluorophores are stable: The loss of fluorescence of adrenolutin amounted to 22% during 180 minutes, and there was no loss of noradrenolutin. For the differentiation of amines, adrenaline was oxidized at pH 2.85 and noradrenaline at pH 7. Precision, accuracy, sensitivity and specifity fulfilled the criteria of analysis. The normal values, determined in a collective of 17 healthy persons, were adrenaline (x +/- s) 44.8 +/- 16.9 nmol/24 h and noradrenaline (x +/- s) 224.0 +/- 68.0 nmol/24h. The simultaneous application of alpha-methyldopa (2 g/day) in 13 patients with primary hypertension did not disturb the fluorimetric estimation of catecholamines.
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PMID:[An improved trihydroxyindole method for the determination of urinary catecholamines]. 0 40

Beta adrenergic receptor antagonists (beta blockers) differ greatly in their cardioselectivity and intrinsic sympathomimetic activity, and these differences may have important therapeutic consequences. We have therefore studied the effect on blood pressure, heart rate and plasma renin activity of the beta blocking drug oxprenolol (Trasicor) which has considerable intrinsic sympathomimetic activity, both alone and in combination with the benzothiadiazine cyclopenthiazide. Eleven patients with mild to moderate benign essential hypertension were randomly allocated to one of two treatment groups. Oxprenolol was given as the first drug to Group 1, and cyclopenthiazide as the first drug to Group 2. The patients were assessed before the start of treatment, after 2 to 3 weeks of treatment with one drug and after a further 2 to 3 weeks of treatment with both drugs. Heart rate, blood pressure and plasma renin activity were measured with the patients recumbent and after a standardized tilt to 85 degrees to provide a reflection of day to day cardiovascular stress. Oxprenolol reduced arterial blood pressure without inducing significant bradycardia. The addition of cyclopenthiazide had little further effect. Oxprenolol alone suppressed plasma renin activity both at rest and during tilt and also abolished the increase in plasma renin activity after administration of cyclopenthiazide. The combination of (1) moderate reduction of blood pressure. (2) inhibition of the otherwise inevitable increase in plasma renin activity with the use of a diuretic drug, and (3) only moderate inhibition of overall sympathetic activity indicates that it is possible to achieve physiologic balance with the appropriate beta blocking drug.
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PMID:Beta adrenergic blockade and diuretic therapy in benign essential hypertension: A dynamic assessment. 0 63

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.
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PMID:Control of renin release: a review of experimental evidence and clinical implications. 0 64

Primary aldosteronism and renovascular hypertension are two different diseases in which renin determinations are necessary for establishment of diagnosis or therapeutic procedure. Low renin values which are not stimulated by acute stimuli combined with elevated plasma aldosterone concentrations confirm the diagnosis of primary aldosteronism. When in a patient with proven renal artery stenosis a significant difference in renal venous renin activity is observed between the two kidneys, a connection between hypertension and renal artery stenosis is likely when in addition the renin secretion of the unaffected kidney is suppressed. A favourable outcome for surgery can be predicted when the individual clinical picture in such a case is also considered. A similar view also holds for the connection between hypertension and unilateral small kidney not due to renal artery stenosis. In essential hypertension the plasma renin level makes it possible to a certain extent to predict whether a patient will benefit from diuretics or from beta-blocking agents. Despite this experience, however, renin determinations are not indicated in every case of essential hypertension. It has not been proven that the prognosis of this disease is improved by renin oriented monotherapy rather than by effective treatment with other antihypertensive agents.
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PMID:[The value of renin determination in the diagnosis of hypertension]. 0 81

Sixteen men with previously untreated essential hypertension in WHO stage I have been studied as out-patients. Oxygen consumption, heart rate (HR), cardiac output (Q) (Cardiogreen) and intraarterial brachial pressure were recorded at rest in supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. The subjects were treated with timolol as the sole drug for one year and the hemodynamic study was repeated. BP was reduced approximately 18% at rest and 14% during exercise, HR approximately 26% and the cardiac index 28% at rest supine and 32% at rest sitting. During exercise the reductions in Q were 25-30%. The calculated total peripheral resistance was significantly increased at rest as well as during exercise. The product of mean arterial pressure and HR was reduced about 40%. No severe side-effects were seen.
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PMID:Hemodynamic long-term effects of timolol at rest and during exercise in essential hypertension. 0 57

In young males with essential hypertension, propranolol and pindolol in small doses caused significant expansion of plasma volume (PV) after one month which did not prevent a reduction in BP. With higher doses, changes in PV were inconsistent and reductions in plasma renin activity (PRA) and 24-hour aldosterone excretion (AE) not closely related to BP changes. The effects of beta-adrenoreceptor blocking drugs on PV, PRA, and AE do not appear to be important components of their anti-hypertensive action.
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PMID:Effects of beta-adrenoreceptor blocking drugs on plasma volume. Renin and aldosterone as components of their antihypertensive action. 0 48

The hypotensive activity of five beta-adrenoceptor antagonists with different ancillary pharmacological properties was compared in a randomised double-blind factorial trial in 25 untreated patients with stable, uncomplicated essential hypertension. In doses that produced similar reductions in exercise tachycardia all drugs had similar blood-pressure lowering activity, greater on systolic than diastolic pressure and greatest during exercise. With the exception of vasodilator activity the possession of any particular combinaton of ancillary pharmacological properties did not significantly influence the specific antihypertensive activity of these compounds.
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PMID:Comparison of antihypertensive activity of beta-blocking drugs during chronic treatment. 0 42

The effects of metoprolol, a selective beta adrenergic receptor antagonist, on blood pressure, beta receptor blockade (antagoinst of isoproterenol and exercise tachycardia), and plasma renin activity (PRA) have been compared with those of placebo in 16 patients with essential hypertension. The dose of metroprolol was 25 mg three times daily for 1 wk and thereafter 100 mg three times daily for 5 wk. The mean decrease in blood pressure during treatment with metoprolol was 24 +/- 3.8 (SEM)/10 +/- 2.1 mm Hg in the lying position and 23 +/- 4.4/9 +/- 3.1 mm Hg after 1 min in the standing position. At a dose of 2.9 to 5.4 mg/kg, steady-state plasma concentrations of metoprolol varied 17-fold (from 20 to 341 ng/ml) between patients and correlated with the interindividual variability in isoproterenol antagonism (r = 0.58, p less than 0.05) and decrease in exercise tachycardia (r = 0.65, p less than 0.01). By contrast, neither of these variables correlated with the dose of metoprolol in mg/kg. Metoprolol decreased PRA by 67 +/- 1.9 and 71 +/- 1.2% in the lying and standing positions, respectively. The decrease in the mean arterial blood pressure in the lying position was significantly correlated to the PRA during the placebo period (r = 0.61, p less than 0.05) but not to the plasma steady-state levels of metoprolol, the degree of beta receptor blockade, and the decrease in PRA.
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PMID:Plasma levels and effects of metoprolol on blood pressure, adrenergic beta receptor blockade, and plasma renin activity in essential hypertension. 0 73

Hemodynamic studies (using (131)I-labeled albumin [RISA]) Were performed before and 5 and 42 weeks after the oral administration of pindolol (av. 30 mg/day), oxprenolol (av. 216 mg/day), propranolol (av. 75 mg/day) or bufetolol hydrochloride (av. 30 mg/day) in 40 patients with essential hypertension. Responders to the antihypertensive actions of short-term (5 weeks) pindolol or bufetolol showed a reduction in total peripheral resistance (pindolol, from av. 2622 to 2022 dyne-sec-cm-5-m2; befetolol, from av. 3301 to 2620, p less than 0.05), without significant changes in cardiac index, while hypotensive actions of propranolol or oxprenolol appeared to be due mainly to a decrease in cardiac output (propranolol, from av. 4.03 to 2.99 L/min/m2; oxprenolol, from av. 3.97 to 3.29 L/min/m2), although the decrease in cardiac output was not significant. In long-term (42 weeks) oxprenolol therapy, antihypertensive effects seemed to be related to reduced cardiac output and a readaptation of peripheral resistance to chronic reduction of cardiac output was not always observed. Circulation time was determined in 9 patients with oxprenolol therapy and 8 with pindolol therapy by the measurement of the arrival time in the cerebral hemisphere of the intravenously injected radioisotope. The patients with oxprenolol therapy showed significant prolongation in circulation time (short-term administration, av. 6.6 to 8.4 sec; long-term administration av. 6.6 to 9.2 sec, p less than 0.05), while no prolongation was observed in pindolol therapy. These results suggest that hemodynamic responses to beta-blocking agents are not uniform and that the antihypertensive actions of beta-blockers depend on the effects on both cardiac output and peripheral vascular resistance.
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PMID:Hemodynamic effects of beta-adrenergic blockade with pindolol, oxprenolol, propranolol and bufetolol hydrochloride in essential hypertension. 0 88


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