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)

Insulin-induced drinking (IID) in male Wistar rats, evoked by administering 5 U/kg of crystalline porcine insulin i.p., was significantly decreased by propranolol (0.1 and 0.5 mg/kg s.c.) after 1 and 2 h. The blood glucose of rats treated with a much higher dose of propranolol (10 mg/kg body weight) and insulin did not differ from that of rats treated solely with insulin after 30 and 120 min. Atenolol (0.5 mg/kg s.c.) caused a reduction in IID after 1 and 2h. Butoxamine (1 mg/kg s.c.) also reduced IID after 1 and 2h, and at 0.5 mg/kg after 1h. The alpha-blocker, phenoxybenzamine (10 mg/kg s.c.), had the opposite effect, stimulating IID after 2h. There is no direct evidence that insulin activated the sympathetic system at the doses used in these experiments. Nevertheless, the results reported here seem to be compatible with the involvement of the sympathetic system in IID, possible through the renin-angiotensin system.
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PMID:Attenuation of insulin-induced drinking by beta-adrenoceptor antagonists. 176 67

The effects of single oral doses of the angiotensin converting enzyme (ACE) inhibitor quinapril (CI-906) 40 mg and the cardioselective beta-adrenoceptor blocker atenolol 100 mg on sympathetic and parasympathetic function and on exercise capacity have been studied in 8 healthy young men. The trial followed a double-blind, placebo controlled, randomized cross-over design, with at least one week between treatments. Blood pressure (BP) and heart rate (HR) at rest were slightly reduced by atenolol but were not affected by quinapril. Atenolol impaired the sympathetically mediated increases in HR and BP caused by standing, immersion of the hand into melting ice, the Valsalva manoeuvre and isometric forearm exercise. Quinapril did not influence those responses nor the vagally mediated bradycardia of the diving reflex. Atenolol, however, augmented the vagal bradycardia, presumably by sympathetic inhibition. In a dynamic bicycle ergometer test with a stepwise increasing work load, exercise performance was decreased by atenolol but not by quinapril. Inhibition of the renin-angiotensin system by quinapril was shown by a marked decrease in serum ACE activity and a several-fold increase in plasma renin activity (PRA). Atenolol produced a moderate reduction in PRA. Before or during exercise, plasma noradrenaline and adrenaline were not influenced by either drug. The results indicate that, unlike the atenolol-induced beta-adrenoceptor blockade, ACE inhibition by a single dose of quinapril had no clear effect on autonomic nervous function or exercise capacity.
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PMID:Effects of single doses of quinapril and atenolol on autonomic nervous function and exercise capacity in healthy volunteers. 219 98

The subcutaneous administration of a single dose of the beta-adrenoceptor antagonists atenolol, betaxolol, oxprenolol, pindolol, propranolol, or sotalol to conscious spontaneously hypertensive rats (SHR) lowered mean arterial pressure (MAP) by 15-20%, but this vaso-depression was not accompanied by a rise in plasma norepinephrine (NE) concentration. When MAP was decreased at the same rate and to the same extent with the vasodilator minoxidil, plasma NE concentration increased 50-75%. Atenolol, betaxolol, propranolol, and sotalol lowered heart rate, whereas oxprenolol, pindolol, and minoxidil elicited a tachycardia. Atenolol (-48%), betaxolol (-63%), and propranolol (-29%) significantly suppressed plasma renin activity (PRA), and minoxidil elevated PRA by 150-315%. Pindolol (+37%) caused a nonsignificant increase in PRA, and oxprenolol (-23%) and sotalol (-17%) produced nonsignificant decreases in PRA. Because the beta-adrenoceptor antagonists did not increase plasma NE concentration, whereas an equivasodepressor dose of minoxidil did, we conclude that plasma NE concentration is inappropriately low relative to the decrease in MAP caused by beta-adrenoceptor antagonists in the conscious SHR. In addition, the diverse effects of the beta-adrenoceptor antagonists on PRA in SHRs indicate that a suppression of renin release cannot account for either the decrease in MAP caused by these drugs or the failure of plasma NE concentration to increase when MAP is decreased by beta-adrenoceptor antagonists.
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PMID:Response of plasma norepinephrine concentration to the vasodepression caused by beta-adrenoceptor antagonists in the conscious spontaneously hypertensive rat. 243 2

The cardioselectivities of five beta-adrenoceptor antagonists were compared. Six normal subjects received, in a double-blind random order, 200 mg acebutolol, 50 mg atenolol, 10 mg betaxolol, 100 mg metoprolol, 80 mg propranolol, and placebo. All beta-adrenoceptor antagonists produced a similar reduction in exercise tachycardia. Isoprenaline infusions in incremental doses were given. Dose-response curves were constructed and the doses of isoprenaline required to increase heart rate by 25 beats/min (I25), forearm blood flow by 3 ml/100 ml/min (IF3), and finger tremor by 200% (IT200), and decrease diastolic blood pressure by 25 mm Hg (ID25), after each treatment were compared. After propranolol, I25, ID25, IF3, and IT200 were greater (p less than 0.02) than after atenolol, betaxolol, and metoprolol; I25, ID25, and IT200 were greater than after acebutolol. After acebutolol I25, ID25, and IF3 were greater than after atenolol and betaxolol; IT200 was greater than after betaxolol. Atenolol and betaxolol caused less reduction in the isoprenaline-induced changes in blood glucose, plasma potassium, lactate, renin activity, and serum insulin than propranolol. Acebutolol caused less attenuation of blood glucose and plasma lactate, and metoprolol less attenuation of plasma renin activity, than propranolol. It is concluded that acebutolol, atenolol, betaxolol, and metoprolol cause less blockade of beta 2-adrenoceptors than propranolol, and atenolol and betaxolol are more cardioselective than acebutolol.
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PMID:A comparison of the cardioselectivity of five beta-adrenoceptor blocking drugs. 244 Nov 75

Adrenergic activity regulates renal function by several mechanisms. Renal nerves not only exert vasoconstrictor functions but also may influence glomerular hemodynamics by beta-adrenergic activity, especially via the effects on renin angiotensin activity. Little is known of the specific glomerular hemodynamic alterations resulting from beta 1-adrenergic blockade. Current studies examined the effects of 4-6 days of treatment with atenolol (50 mg/kg), a beta 1-selective adrenergic antagonist, on glomerular hemodynamics in plasma volume-expanded Munich-Wistar rats. Atenolol treatment reduced blood pressure both in the awake state and during micropuncture. This reduction in blood pressure contributed to a decrease in nephron filtration rate (48 +/- 1 in untreated rats vs. 40 +/- 1 nl.min-1.g kidney wt-1 in the atenolol-treated group, P less than 0.05) by reduction in nephron plasma flow (182 +/- 2 vs. 154 +/- 4 nl.min-1.g kidney wt-1 in the atenolol-treated rats). No other determinant of glomerular ultrafiltration was influenced by atenolol treatment. Since beta 1-adrenergic blockade may influence the generation of angiotensin II, the response to angiotensin II infusion was assessed and found not to differ from control untreated animals. These studies demonstrate that beta 1-receptor blockade reduced nephron filtration rate by decreasing mean arterial blood pressure and nephron plasma flow without significant modifications in vascular resistance and the glomerular hydrostatic pressure gradient.
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PMID:Effects of beta 1-adrenergic blockade on glomerular dynamics and angiotensin II response. 254 99

Experimental and clinical evidence indicates that cardiac hypertrophy in systemic hypertension may not simply result from the mechanical stress of increased afterload. Several lines of evidence suggest that sympathetic nervous influence stimulates cardiac growth. A previous study indicated that sympathetic tone may be important in the two-kidney, one-clip model of renovascular hypertension. Hence, we investigated the role of cardiac beta-receptors by testing the effects of the cardioselective beta-receptor blocker, atenolol, on regression and prevention of ventricular hypertrophy in this model. Renal hypertensive rats were assigned to a 'prevention' and a 'reversal' protocol, receiving the drug before or after the development of hypertension and cardiac hypertrophy. Untreated control animals developed severe hypertension (205 +/- 9 mmHg) and marked cardiac hypertrophy (heart weight/body weight ratio: 3.86 +/- 0.23 mg/g) when compared to sham-operated controls (129 +/- 1 mmHg and 2.38 +/- 0.06 mg/g, respectively). Atenolol (440 mg/kg per day) failed to prevent or reverse hypertension (213 +/- 5 and 194 +/- 11 mmHg) or cardiac hypertrophy (4.10 +/- 0.39 and 3.51 +/- 0.25 mg/g, respectively). Effective beta-blockade was verified by significantly lower heart rates in treated animals (382 +/- 10 and 368 +/- 9 beats/min, respectively) than untreated controls (486 +/- 28 beats/min; P less than 0.01). Similarly, plasma renin activity returned to baseline in atenolol-treated animals. Cardiac catecholamines were markedly decreased in hypertrophied hearts (significant only for norepinephrine) and remained unaffected by atenolol treatment. However, both the prevention and reversal protocol strikingly reduced mortality in hypertensive animals (0 and 14%, respectively, versus 57%; P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of beta 1-adrenoceptors in hypertensive cardiac hypertrophy. 282 68

In order to assess whether blood pressure reduction with atenolol or enalapril is associated with changes in renal prostaglandin (PG) synthesis, we studied the effects of 10 weeks therapy in 20 subjects with mild or moderate hypertension. After a four week placebo run-in period, subjects were randomized to receive either atenolol 50-100 mg/day or enalapril 5-20 mg/day for 10 weeks, then crossed over to the alternate active drug. Both drugs lowered blood pressure: placebo 147/97, atenolol 135/87, enalapril 132/87 (p less than 0.05, for both). Atenolol reduced resting heart rate but neither drug changed body weight, serum sodium or potassium or creatinine clearance. Intravenous furosemide was used as a standardized stimulus of renal PG synthesis. Neither drug changed the excretion rates of 6ketoPGF1 alpha or thromboxane B2 (hydrolysis products of PGI2 and thromboxane A2 respectively). Diuretic, kaliuretic, and natriuretic effects of furosemide were also not affected. Plasma renin activity was increased by enalapril but reduced slightly by atenolol. Subjects with more marked blood pressure reduction showed responses to furosemide no different than those with less effect. We conclude that blood pressure reduction with atenolol or enalapril does not change the response of renal eicosanoid synthesis to acute stimulation with furosemide.
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PMID:Effects of atenolol and enalapril on blood pressure, plasma renin activity and urinary prostanoids. 284 Oct 53

The influence of chronic beta 1-adrenoceptor blockade on haemodynamic and metabolic responses was examined in eight young hypertensive subjects during a 40 min submaximal bicycle test at 50% of maximal capacity. The patients were randomly allocated to one placebo and one treatment period of 6 weeks. During treatment atenolol (Tenormin, 100 mg) was given twice daily. Arterial pressure, cardiac output, leg blood flow, oxygen uptake and different metabolites in the blood were determined. The heart rate was reduced by beta 1-adrenoceptor blockade by 30% during exercise, and the decrease was related to plasma concentration of the drug. Cardiac output was decreased by approximately 10%, but the negative chronotropic effect was partly compensated for by a higher stroke volume. Blockade leg blood flow was reduced by 10%, but more oxygen was extracted, giving an unchanged oxygen uptake. Blood concentration and leg uptake of glucose were not influenced by the treatment, but plasma free fatty acids were reduced by 30-40%. Leg lactate release was decreased to half the value in the unblocked situation. Plasma renin activity did not increase at the beginning of exercise, but after 40 min an increase was seen, though only to half of the pretreatment value. It is concluded that beta 1-adrenoceptor blockade during submaximal exercise reduces blood flow to the working muscles and that this reduction is the result of a lower cardiac output. Aerobic metabolism is unchanged as a result of increased oxygen extraction, but less fat is used as lipolysis is inhibited. Glucose uptake by the working muscles is unchanged by beta 1-blockade, but there is evidence for an increased carbohydrate metabolism. As for non-selective blockade, atenolol decreases lactate release but this could be the result of non-specific action on the beta 1-receptor and/or increased carbohydrate oxidation. Furthermore, the beta 1-adrenoceptors seem to have a major influence on the renin release during exercise.
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PMID:Haemodynamic and metabolic responses to prolonged exercise after chronic beta 1-adrenoceptor blockade in hypertensive man. 286 Sep 92

The 15-20% decrease in mean arterial pressure (MAP) seen in conscious spontaneously hypertensive rats (SHR) after the administration of a single dose of the beta-adrenoceptor antagonists atenolol, betaxolol, oxprenolol, pindolol, propranolol or sotalol was not accompanied by an increase in plasma norepinephrine (NE) concentration. In marked contrast, plasma NE concentration increased by 50-75% when MAP was lowered at the same rate, and to the same extent with the vasodilator minoxidil. Atenolol, betaxolol and propranolol significantly suppressed plasma renin activity (PRA), whereas oxprenolol, pindolol and sotalol did not alter PRA significantly. Based on these observations, I conclude that beta-adrenoceptor antagonists impair the normal baroreflexly-mediated increase in plasma NE concentration which occurs in response to a decrease in MAP and this sympatho-inhibitory effect does not require the suppression of renin release.
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PMID:The response of plasma catecholamines to the vasodepression caused by beta-adrenoceptor antagonists in the spontaneously hypertensive rat. 287 69

Activation of the renin-angiotensin-aldosterone system has been hypothesized as a potential pathophysiological factor in premenstrual tension syndrome (PMS). Atenolol is a predominate beta 1-blocker which can decrease plasma renin activity and inhibit the urinary excretion of aldosterone. Sixteen women meeting provisional diagnoses of late luteal phase dysphoric disorder were treated for symptoms of PMS with atenolol (50 mg once daily) in a randomized placebo-crossover double-blind design. The data indicated significant improvements on the irritability, vigor, elation, and friendliness scores in response to atenolol compared to placebo. Significant changes were not found for several other ratings scales, indicating that atenolol improved only selected symptoms in the group as a whole. However, the women who had premenstrual tension symptoms for more than 5 years (n = 8) were improved on most of the rating scales. Atenolol decreased premenstrual plasma aldosterone to a limited extent. There was also a trend in the data toward higher luteal progesterone levels during the month subjects took atenolol. Plasma renin activity and aldosterone correlated with estrogen and progesterone levels during the placebo month but not during the active month.
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PMID:Atenolol treatment of late luteal phase dysphoric disorder. 297 84


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