Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of labetalol, an alpha- and beta-adrenoceptor antagonist, on maximum exercise heart rate and on plasma renin, aldosterone, noradrenaline, and adrenaline levels at rest and during exercise in hypertensive patients. The dose of labetalol was doubled weekly from 0.3 to 2.4 g per day. The maximum exercise heart rate fell significantly during labetalol treatment, and there was a significant correlation between exercise tachycardia and the dosage of labetalol. Plasma renin activity and aldosterone concentration at rest decreased during treatment with labetalol. The exercise-induced increase in plasma renin activity was reduced by labetalol. Labetalol did not cause any significant changes in plasma noradrenaline and adrenaline at rest or during exercise.
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PMID:Effects of labetalol on plasma renin, aldosterone, and catecholamines in hypertensive patients. 9 28

1. Labetalol was administered to 18 hypertensive patients for an average duration of 2.44 weeks, with an average final daily dose of 1.65 g. 2. Labetalol decreased resting heart rate by 16% and maximal exercise heart rate by 21%; the phenylephrine-induced rise of systolic brachial artery pressure was reduced by 36%. 3. During labetalol brachial artery pressure was lowered by 29/15 mmHg in the recumbent position, by 41/23 mmHg at rest sitting, and by 53/23 mmHg at maximal exercise; total peripheral resistance was not significantly affected at rest recumbent, but was reduced at sitting and at exercise; cardiac output decreased in all conditions. 4. Labetalol reduced mean pulmonary artery and capillary wedge pressures only in the sitting position. Pulmonary vascular resistance remained unchanged. 5. The drug produced significant decreases of plasma renin activity and of plasma aldosterone concentration.
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PMID:Effects of labetalol on systemic and pulmonary haemodynamics at rest and during exercise in hypertensive patients. 28 68

1 Bendrofluazide (10 mg/day) or labetalol (300 mg and 600 mg/day) produced significant reductions in lying, standing, and post-exercise blood pressure in ten hypertensives. 2 Active treatments were approximately equivalent in anti-hypertensive effect. However, comparing lying and standing determinations, labetalol (600 mg/day) produced significantly greater additional postural falls in systolic blood pressure than during placebo or bendrofluazide treatment. 3 Systolic blood pressure rose after exercise during placebo or bendrofluazide treatment. However, on labetalol, mean changes in systolic blood pressure after exercise were negative and significantly different from those seen on placebo. 4 Greater reductions in lying and post-exercise systolic blood pressure were produced by combination treatment than by either individual drug. Additional postural and exercise-related falls in systolic blood pressure tended to be smaller with combination treatment than during treatment with labetalol alone. 5 Labetalol significantly reduced lying, standing, or post-exercise heart rate by comparison with placebo or bendrofluazide. 6 Labetalol significantly reduced lying, standing, or post-exercise heart rate by comparison with placebo or bendrofluazide. 6 Labetalol moderately reduced plasma renin activity, whereas bendrofluazide caused marked elevation. The effect of bendrofluazide predominated during combination treatment.
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PMID:A comparison of the effects of labetalol, bendrofluazide and their combination in hypertension. 38 23

1. Four different doses of labetalol (150, 300, 600 and 900 mg/day) were given for 1 week to each of four groups of patients with essential hypertension (six patients for each group). 2. Labetalol decreased mean blood pressure and heart rate to the same extent on the first and the seventh days of treatment. Only standing blood pressure showed a dose-dependent inhibition both in the supine and upright position. 3. Labetalol exerted a net inhibitory effect on plasma renin activity, which was related to basal renin values and was already maximal at the lowest doses. This effect was well maintained in the supine position. This effect was well maintained in the supine position, although during standing it tended to be less evident with increasing doses. 4. Urinary aldosterone was decreased in a dose-dependent fashion and its changes were largely independent fashion and its changes were largely independent of plasma renin activity. 5. Neither basal values nor changes of renin and aldosterone were related to the hypotensive effect of labetalol. 6. During labetalol treatment urinary sodium excretion fell for 2-3 days and then returned to basal values. The retentive effect of labetalol on sodium was directly related to the decrease of blood pressure, and the successive sodium escape might be explained either by the observed increase of plasma volume (indirectly measured by packed cell volume) or by aldosterone inhibition.
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PMID:Effect of increasing doses of labetalol on blood pressure, plasma renin activity and aldosterone in hypertensive patients. 39 86

The effects of intravenously administered labetalol on blood pressure and pulse rate were examined in 17 patients with severe hypertension. Prompt and sustained falls in supine blood pressure and pulse rate occurred in ten patients (responders), but seven patients showed little or no change in either measurement (non-responders). Labetalol had a more marked effect on standing than on supine blood pressure. Only two of the responders, but all of the non-responders were concurrently receiving antihypertensive drugs. Plasma renin activity, plasma renin concentration and plasma angiotensin II concentration fell slightly over the one-hour period of observation in ten patients in whom serial measurements were made, but the changes were independent of the blood pressure response.
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PMID:Emergency treatment of severe hypertension with intravenous labetalol. 73 28

In so-called essential hypertension, at least three different subsets of pathophysiologic findings can be identified: mild hypertension in nonobese juvenile subjects characterized by elevated cardiac output, normal peripheral resistance, increased sympathetic activity as measured by norepinephrine and plasma renin activity; hypertension in the elderly with a low cardiac output, often with left ventricular hypertrophy, elevated total peripheral resistance, nephrosclerosis contracted intravascular volume, and low plasma renin activity; and obese hypertensive patients with a high cardiac output, expanded intravascular volume, and a normal total peripheral resistance. Although there is often an overlap among these three entities, antihypertensive treatment can easily be adapted accordingly. A beta-adrenoreceptor blocker is the step-one drug to be used in mild hypertension with an elevated cardiac output. The drug's negative inotropic and chronotropic properties will bring the elevated cardiac output and heart rate back to normal. In the elderly hypertensive patient, an arteriolar and venous vasodilator, such as an antiadrenergic agent, slow channel calcium blocker, or a converting enzyme inhibitor, will lower total peripheral resistance and unburden the left ventricle. In the obese patient and also in most black subjects, the first-step antihypertensive agent remains a thiazide diuretic. Labetalol, an agent with both beta- and alpha-adrenoreceptor properties, shows promise for the treatment of hypertension in the young as well as in the older patient. It seems to be the agent of choice in patients with established essential hypertension who are concomitantly suffering from coronary artery disease.
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PMID:Hemodynamic and cardiac adaptation in essential hypertension. Consequences for therapy. 242 59

Hypertension after carotid endarterectomy has a variable incidence ranging up to 56%. Blood pressure (BP) control is essential due to possible increased risk of morbidity from neurologic deficits or cardiovascular complications. This study evaluated intravenous labetalol for control of hypertension after carotid endarterectomy. Sixty ASA II-IV patients were studied; 20 developed BP high enough for treatment with labetalol. The anesthetic technique was standardized. Labetalol was administered at the conclusion of surgery as a 20-mg bolus over two minutes followed by 40 mg every 10 minutes until the desired BP was achieved (BP less than or equal to 10% above average preoperative BP or less than 150 mmHg, systolic) or 300 mg had been given. The mean total dose of labetalol was 42.0 +/- 33.0 mg (mean +/- SD) and mean time to reach the desired BP was 16.2 +/- 21.4 minutes. Systolic, diastolic, mean arterial pressure and heart rate significantly decreased after labetalol treatment and remained so for the remainder of the 180-minute study period. There was no hypotension, bradycardia, evidence of myocardial ischemia or central nervous system dysfunction present with labetalol treatment. Blood samples were obtained for determination of plasma renin activity, epinephrine, and norepinephrine in 10 patients who developed hypertension and received labetalol, and 10 patients who did not develop hypertension. In the patients developing hypertension, there was a significant elevation in epinephrine just before treatment, that decreased by 30 minutes after treatment. Norepinephrine levels became significantly elevated five minutes after labetalol treatment in the group with hypertension and remained elevated for 120 minutes. Concomitantly, there was a significantly lower plasma renin activity seen in this group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous labetalol for the treatment of hypertension after carotid endarterectomy. 257 2

The present review shows that labetalol has many advantageous properties in the treatment of patients suffering from angina pectoris with or without hypertension. These patients respond with vasoconstriction to a variety of internal and external influences. The selective alpha 1-blocking component in addition to the non-selective beta-blockade of labetalol attenuates the increased coronary vascular resistance and improves coronary haemodynamics especially under stress in a manner which should be favourable in myocardial ischaemia. In addition, the alpha 1-blocking component may prevent different kinds of arrhythmias generated by alpha-adrenoceptor stimulation. Labetalol has no effect on renal blood flow, glomerular filtration rate, plasma electrolyte concentrations, glucose tolerance, lipoprotein cholesterol ratio, renin-angiotensin-aldosterone system, uric acid levels, or on platelet aggregation. Intravenously administrated labetalol has proved to be effective in patients with acute myocardial infarction, especially if associated with hypertension. In order to avoid postural hypotension, oral treatment should be started with a low dose of 100 mg twice daily. The usual dosage in patients without hypertension is 200 mg twice daily, but in patients with hypertension doses up to 1200 mg or even more have been used. In low doses up to 400 mg daily, the unwanted effects are few and often self-limited. High doses can cause side effects related to both beta- and alpha-blocking properties of labetalol. As an antianginal agent labetalol has proved to be at least as effective as selective or non-selective beta-blockers.
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PMID:Labetalol in the treatment of angina pectoris. 288 99

The effects of labetalol on the secretion of prostacyclin and plasma-renin activity (PRA) were evaluated, relative to a control group in 24 patients undergoing hip osteotomy. They were randomly assigned to two groups (G-I and G-II) with 12 patients each. Patients allocated to both groups received standard anaesthesia (thiopentone, pancuronium, fentanyl and nitrous oxide). Patients belonging to Group II were given labetalol at a dose of 0.8 mg kg-1. The stable metabolite of PGI2, 6-keto-PGF1 alpha was quantified from urine samples by radioimmunoassay (RIA). Cortisol, PRA and aldosterone were determined from blood samples. A significant increase in 6-keto-PGF1 alpha elimination was observed in G-I. Labetalol administration partially but significantly inhibited this increase. We believe that prostacyclin is involved not through the beta 1 but through the alpha 1 receptors in the secretion of renin.
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PMID:The effect of labetalol on urinary prostacyclin secretion during surgery. 353 90

Two separate randomized double-blind, crossover trials were carried out in hypertensive patients to evaluate the antihypertensive efficacy and safety of verapamil. In the first study, verapamil, in doses of 120 mg three times daily, was compared with pindolol, in doses of 7.5 mg twice daily. A thiazide diuretic was given with both drugs. In another study, verapamil, in doses of 160 mg twice daily, was compared with 200 mg twice daily of labetalol in hypertensive patients with coexisting chronic obstructive lung disease. Blood pressure fell equally with these drugs, and neither of the drugs caused significant side effects. Labetalol significantly reduced both forced expiration volume at 1s (FEV1) and forced vital capacity (FVC), suggesting a bronchoconstrictor effect. Verapamil was devoid of any such effect. Verapamil did not affect plasma renin concentration.
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PMID:Evaluation of verapamil in the treatment of hypertension. 354 Feb 29


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