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PubMed1980

Chronic propranolol treatment blunts right ventricular hypertrophy in rats at high altitude.

Chronic beta-receptor blockade has been reported to inhibit right ventricular hypertrophy in rats at high altitude. If so, we wanted to determine whether beta-receptor blockade or some other drug action were involved and whether the heart, the lung vessels, or blood alterations were affected. In rats, chronic treatment with DL-propranolol (2 mg/kg ip once daily) reduced right ventricular hypertrophy and polycythemia of chronic high altitude. D-Propranolol and metoprolol did not reduce hypoxia-induced right ventricular hypertrophy or polycythemia. In isolated lungs from low-altitude rats treated chronically with DL-propranolol or with D-propranolol the pressor response to acute hypoxia was blunted. Chronic DL-propranolol blunted the acute hypoxic pressor response and angiotensin II induced vasoconstriction in lungs from high-altitude rats. Two effects of DL-propranolol treatment were seen: 1) blockade of beta 2-adrenergic receptors, which reduced the right ventricular hypertrophy of high altitude through reduction of hematocrit; and 2) a non-beta-effect, which reduced vascular responsiveness to acute hypoxia in the isolated lung preparation.

Adaptation, Physiological↗
PubMed1982

Propranolol uptake by dog lung: effect of pulmonary artery occlusion and shock lung.

First-pass lung uptake of propranolol in catheterized ambulant dogs was measured by comparison the difference between the ratios of [14C]propranolol to indocyanine green (ICG) before and after a single passage through the pulmonary circulation. Uptake was 56 +/- 5, 53 +/- 8, and 61 +/- 10% (mean +/- SD) when 0.02, 0.2, and 2.0 mg of propranolol were injected, respectively. There was a negative though unimportant correlation between percent uptake and cardiac output. Analysis of paired propranolol and ICG outflow curves confirmed the lack of saturation with increasing dose and suggested the involvement of simple diffusion. In four dogs uptake fell from 4.76 +/- 6.8 to 40.4 +/- 8.2% (0.05 greater than P greater than 0.025) during partial occlusion of the pulmonary circulation by a Swan-Ganz catheter balloon and rose again to 51.2 +/- 6.4% after relief of the occlusion. Propranolol uptake, measured serially in five dogs with indwelling catheters, was initially 55% but fell linearly to 30% over 2 wk (r = -0.59, P less than 0.001), and necropsy showed pathological features of shock lung. A similar study performed on three dogs within 4 days of catheterization showed no change in uptake of the drug. Propranolol uptake appears to reflect both quantitative and qualitative changes in the pulmonary endothelium. This method may therefore be valuable in studying the pulmonary endothelium in health and disease.

Animals↗
PubMed1986

Propranolol does not impair exercise oxygen uptake in normal men at high altitude.

Decreased maximal O2 uptake (VO2max) and stimulation of the sympathetic nervous system have been previously shown to occur at high altitude. We hypothesized that tachycardia mediated by beta-adrenergic stimulation acted to defend VO2max at high altitude. Propranolol treatment beginning before high-altitude (4,300 m) ascent reduced heart rate during maximal and submaximal exercise in six healthy men treated with propranolol (80 mg three times daily) compared with five healthy subjects receiving placebo (lactose). Compared with sea-level values, the VO2max fell on day 2 at high altitude, but the magnitude of fall was similar in the placebo and propranolol treatment groups (26 +/- 6 vs. 32 +/- 5%, P = NS) and VO2max remained similar at high altitude in both groups once treatment was discontinued. During 30 min of submaximal (80% of VO2max) exercise, propranolol-treated subjects maintained O2 uptake levels that were as large as those in placebo subjects. The maintenance of maximal or submaximal levels of O2 uptake in propranolol-treated subjects at 4,300 m could not be attributed to increased minute ventilation, arterial O2 saturation, or hemoglobin concentration. Rather, it appeared that propranolol-treated subjects maintained O2 uptake by transporting a greater proportion of the O2 uptake with each heartbeat. Thus, contrary to our hypothesis, beta-adrenergic blockade did not impair maximal or submaximal O2 uptake at high altitude due perhaps to compensatory mechanisms acting to maintain stroke volume and cardiac output.

Adult↗
PubMed2004

Inhibition of (-)-propranolol hydrochloride by its enantiomer in white mice--a placebo-controlled randomized study.

BACKGROUND: A previous pilot study was performed to see if toxicity of (S)-(-)-propranolol hydrochloride may be inhibited by a potentized preparation of its enantiomer. The present study is based on the hypothesis that the toxic effects of an optical isomer, may be counteracted or reversed by the administration of a potentized preparation of one of its stereoisomers, and in particular the enantiomer. METHODS: 508 ICR conventional mice were used. 254 mice were administered (R)-(+)-propranolol HCl homeopathic potency prior to and during the experiment, and the other 254 were administered indistinguishable placebo. On the day of the experiment mice were anesthetized with intraperitoneal Rometar. Once sedated the mice were administered the LD50 dose of (-)-propranolol HCl intraperitoneally. RESULTS: The end point for statistical analysis was the difference in survival between the placebo and treatment mice. The odds ratio for survival of treatment mice relative to placebo mice was 1.52. The hypothesis of equal survival proportions gave a chi-square of 5.0429 (1 degree of freedom), which has a p-value of 0.0247. The analysis was then adjusted for mouse weight and intraperitoneal (-)-propranolol dosage using a logistic regression (LR) model. The LR treatment odds ratio was 1.51 and the LR treatment chi-square was 4.8112 (1 degree of freedom), which has a p-value of 0.0283. Consequently, we reject the null hypothesis of no treatment effect on survival. Eleven percent more treatment mice survived than placebo mice. CONCLUSION: We conclude that the toxicity of intraperitoneal (-)-propranolol HCl, may be counteracted by administration of a potency of its enantiomer, in ICR conventional mice which have survived preceding intraperitoneal Rometar injection, and pre-dosing with (+)-propranolol HCl homeopathic potency.

Adrenergic beta-Antagonists↗
PubMed1997

Propranolol as an adjunct therapy for hyperthyroid tremor.

We evaluated the use of propranolol as an adjunct to carbimazole in the treatment of hyperthyroid tremor and tachycardia in a double-blind, cross-over and placebo-controlled study. Seven patients were given carbimazole plus either placebo or propranolol (40 mg) for 1 month and then switched to the alternative adjunct treatment for a further month. All patients showed significant improvements (p < 0.001) of heart rate and tremor amplitude after 1 or 2 months from baseline. One month after the baseline, the mean improvements of heart rate were 23% for the carbimazole + placebo group and 38% for carbimazole + propranolol group. Tremor also improved during the 1st month of the study by 31% in the carbimazole + placebo group versus 59% in the carbimazole + propranolol group. Whereas further improvements were observed in both variables in those receiving propranolol as the second adjunct treatment, this was not the case in those who received placebo during the same period. These findings confirm that the beta-blocker propranolol is a useful adjunct in the early treatment of both the tremor and tachycardia of hyperthyroidism.

Adrenergic beta-Antagonists↗
PubMed1981

Effects of reserpinization, surgical denervation and in vitro chemical denervation with 6-hydroxydopamine on the contractile response of isolated rabbit ear artery to propranolol.

The contractile effect of propranolol in isolated rabbit ear artery was assessed in reserpinized and in surgically and chemically denervated blood vessels. Reserpinization and surgical denervation either had no effect on or enhanced the ear artery contractile response to 10(-6) to 10(-4) M propranolol. In contrast, the contractile response to propranolol was nearly abolished after denervation of the ear artery in vitro with 6-hydroxydopamine (6-OHDA). Dose-response curves to norepinephrine were shifted to the left by factors of 4.9 in 6-OHDA denervated ear arteries and 15.6 in untreated arteries in the presence of 10(-7) M desipramine. The diluent for 6-OHDA shifted both the norepinephrine and propranolol dose-response curves to the right. It is proposed that propranolol caused a contractile response in ear artery by an action on the postsynaptic tissues of this vessel. 6-OHDA denervation caused nonspecific desensitization in rabbit ear artery leading to the loss of response of this vessel to propranolol.

Animals↗
PubMed1986

Developmental changes in the effects of beta-adrenergic blocking concentrations of propranolol on canine Purkinje fibers.

We used standard microelectrode techniques to investigate the developmental changes in the effects of the beta-blocker propranolol on canine Purkinje fibers. The effects of propranolol on the transmembrane action potential were similar in neonatal and adult Purkinje fibers. In automatic Purkinje fibers we obtained concentration-response (increase in rate) curves for isoproterenol alone and with an increasing concentration of propranolol. The curve for isoproterenol in neonatal Purkinje fibers had an EC50 of 1.0 X 10(-9) M, about 5-fold lower than in adult Purkinje fibers (EC50 = 5.03 X 10(-9) M, p less than 0.05). At both ages, propranolol caused a parallel, concentration-dependent shift of the response curves for isoproterenol, with no change in the maximum effect. Equiactive dose ratios in presence and absence of 3 concentrations of propranolol were compared by the Schild plot. The pA2 values for adult and neonate Purkinje fibers were 8.32 (8.14-8.46; 95% confidence level) and 8.86 (8.69-9.03; 95% confidence level), respectively. Our results indicate significant (p less than 0.05) developmental changes in the beta-blocking effects of propranolol in canine Purkinje fibers.

Action Potentials↗
PubMed1978

Beneficial actions of N-dimethyl propranolol on myocardial oxygen balance and transmural perfusion gradients distal to a severe coronary artery stenosis in the canine heart.

The purpose of the present study was to compare the effects of N-dimethyl propranolol (DMP), the quaternary derivative of propranolol, and propranolol on the transmural distribution (endo/epi) of coronary blood flow in normal and ischemic regions of the myocardium. The distribution of blood flow between subendocardium and subepicardium of a nonischemic region and one distal to a severe left circumflex coronary artery stenosis was determined by use of tracer microspheres (15 microgram) in intact dog hearts. DMP (1,5 and 10 mg/kg I.V.) produced a small dose-related increase in endo/epi of the nonischemic region (1.15 +/- 0.04--1.24 +/- 0.05), whereas a larger increase was observed in the ischemic region (0.61 +/- 0.08--1.09 +/- 0.10). DMP also produced a significant increase in ischemic subendocardial blood flow (0.59 +/- 0.12--0.76 +/- 0.11 ml/min/g). Similarly, propranolol (0.5 and 1.0 mg/kg I.V.) produced a small increase in endo/epi of the nonischemic region (1.18 +/- 0.08--1.30 +/- 0.07) and a larger increase in the ischemic region (0.72 +/- 0.17--1.18 +/- 0.09). However, propranolol did not increase ischemic subendocardial blood flow. It is concluded that DMP may be an alternative to propranolol in certain types of acute myocardial ischemia when beta-adrenergic blockade is undesirable.

Animals↗
PubMed1980

The effect of concurrent oral administration of propranolol and disopyramide on cardiac function in healthy men.

Sixteen healthy men were evaluated for left ventricular performance changes and beta-blockade after therapeutic oral doses of disopyramide and propranolol administered alone and concurrently. The volunteers were randomly assigned to receive one of two drug treatment regimens that differed in the sequence and duration of administration of the drugs. Left ventricular function was assessed by echocardiographically determined ejection fraction (EF) and systolic time intervals. Beta-blockade was assessed by changes in exercise heart rate. Both disopyramide and propranolol exhibited negative inotropic activity, as evidenced by significant, although clinically inconsequential, decreases in EF and increases in the ratio of preejection period to left ventricular ejection time. The negative inotropic effects of a single 200-mg dose of disopyramide and an 80-mg dose of propranolol were comparable, while chronic disopyramide therapy (200 mg every 6 hours for 1 week) had a greater negative inotropic effect than chronic propranolol therapy (80 mg every 8 hours for 1 week). Only propranolol had beta-adrenoceptor blocking activity. When the drugs were administered concurrently, the negative inotropic effects of oral propranolol and disopyramide were neither additive nor synergistic.

Administration, Oral↗
PubMed1980

Adrenergic responsiveness after abrupt propranolol withdrawal in normal subjects and in patients with angina pectoris.

Adrenergic responsiveness after abrupt propranolol withdrawas during exogenous and esdogenous catecholamine stimulation was assessed in 10 normal subjects and 10 patients with angina pectoris. Propranolol, 160 mg/day, was administered for 2 weeks and then stopped. During an epinephrine infusion, period (p < 0.005). There were no differences from control 96 hours after the drug had been stopped in both groups or at 144 hours in the angina patients who were studied for a longer time. At 48 hours of heart rate and the pressure-rate product were significantly less than control level in the angina patient, but not in the normal subjects. Similar results were observed during exercise in both groups. The epinephrine-induced increase in free fatty acids was blocked by propranolol (p < 0.005), was still attenuated at 48 hours of withdrawals (p < 0.05), but returned to control levels thereafter in both groups. Resting serum triiodothyromine levels decreased with propranolol ( < 0.005) and remaind low throughout the withdrawal period. Measurements of dopamine beta-hydroxylase, plasma platelet factor 4, and platelet aggregation at rest and after exercise did not change significantly during or after propranolol administration. Plasma norepinephrine and epinephrine values were not changed from control during the withdrawal period at rest or after exerise. We conclude that there is no evidence of hypersensitivity to beta-adrenergically mediated responses after abrupt propranolol withdrawal.

Adult↗
PubMed1981

Effect of oral propranolol on rest, exercise and postexercise left ventricular performance in normal subjects and patients with coronary artery disease.

The effect of beta-adrenergic blockade with oral propranolol on resting, exercise and postexercise ventricular performance was evaluated using multiple-gated equilibrium cardiac blood and pool images in normal volunteers and patients with coronary artery disease. Propranolol produced no detectable effect on basal left ventricular function in normal subjects at doses producing intermediate (160 mg propranolol/day) and maximal (434 +/- 99 mg propranolol/day) beta blockade and in patients with coronary artery disease at clinically effective antianginal doses (162 +/- 47 mg propranolol/day). During exercise, a dose-related, negative inotropic effect was observed in normal subjects: 160 mg propranolol/day produced a small but statistically insignificant decline in exercise left ventricular performance, whereas maximal beta blockade significantly depressed the left ventricular response to exercise. In patients with coronary artery disease, propranolol's effect on exercise ventricular performance depended on the presence or absence of ischemic dysfunction during exercise. In patients with an ischemic functional response to exercise, propranolol significantly improved regional and global performance during and after exercise; in coronary artery disease patients with a normal response to exercise, propranolol had no significant effect on exercise and postexercise ventricular function. These results imply increased sensitivity to the effects of beta blockade in ischemic myocardium. In coronary artery disease patients with an abnormal response to exercise and in normal volunteers during beta blockade, propranolol's effect on exercise left ventricular performance was independent of changes in ventricular preload and after load related to heart rate and blood pressure.

Administration, Oral↗
PubMed1982

Effects of propranolol therapy on platelet release and prostaglandin generation in patients with coronary heart disease.

Suppression of platelet function is thought to be a mechanism of propranolol's beneficial action in angina pectoris. To study the effects of propranolol on platelets, we measured plasma beta thromboglobulin and plasma thromboxane B2 (TXB2, stable metabolite of TXA2) levels by radioimmunoassay as indexes of platelet alpha-granule and TXA2 release, respectively. Platelet TXA2 generation in vitro in response to arachidonate and thrombin was also quantitated. Twenty-nine patients with coronary disease -- 15 not taking propranolol (group A) and 14 taking propranolol (group B) -- and 15 normal subjects were studied. Plasma beta-thromboglobulin levels were increased in group A and B patients (mean 63 +/- 8 and 96 +/- 14 ng/ml, respectively) compared with normal subjects (mean 46 +/- 6 ng/ml). Plasma TXB2 levels were similar in group A and B patients and in normal subjects (mean 148 +/- 41, 149 +/- 36 and 216 +/- 39 pg/ml). Arachidonate-induced platelet TXA2 generation was significantly higher in group A patients than in normal subjects (725 +/- 393 vs 82 +/- 25 pg TXB2/10(8) platelets, p less than 0.001). In contrast, platelets from group B patients had very low TXA2 generation (mean 21 +/- 18 pg) compared with platelets from group A patients or normal subjects (p less than 0.001). Similar results were obtained using thrombin. These data show that propranolol therapy does not affect platelet-released beta thromboglobulin or TXA2 at rest, but significantly reduces the capability of platelets to generate TXA2 in vitro. Reduction in platelet TXA2 generation may be an important mechanism of action of propranolol in patients with coronary artery disease.

Adult↗
PubMed1993

Propranolol and lidocaine inhibit neural norepinephrine release in hearts with increased extracellular potassium and ischemia.

BACKGROUND: Propranolol and lidocaine are effective antiarrhythmic drugs in myocardial ischemia and infarction. As sympathetic nerve activation and norepinephrine release in ischemic hearts are arrhythmogenic, we tested the possibility that both agents inhibit neural norepinephrine release following sympathetic activation in the ischemic environment. METHODS AND RESULTS: The model used was an in situ perfused innervated rat heart. Norepinephrine release was induced by electrical stimulation of the left cervicothoracic stellate ganglion and analyzed using radioenzymatic assay or high-performance liquid chromatography. In normoxically perfused hearts, evoked norepinephrine release was not affected by either of the two agents at doses of 1 to 10 mumol/L when extracellular K+ concentration was 4 mmol/L but dose-dependently reduced at 10 mmol/L K+ (D,L-propranolol: -53 +/- 4% at 1 mumol/L and -64 +/- 6% at 10 mumol/L K+, lidocaine: -37 +/- 11% at 0.1 mumol/L, -67 +/- 5% at 1 mumol/L, and -75 +/- 6% at 10 mumol/L). At 10 mmol/L K+, norepinephrine release was not affected by timolol or atenolol (both 10 mumol/L but was equally inhibited by D- or L-propranolol at 10 mumol/L (-56 +/- 5% and -53 +/- 9%, respectively), indicating a beta-blocking-independent mechanism. In hearts with metabolic acidosis (pH 6.85) at K+ of 4 mmol/L, neural norepinephrine release was also reduced by propranolol at 10 mumol/L (-37%). Finally, in hearts perfused with 4 mmol/L K+ and subjected to 6-minute periods of ischemia, neural norepinephrine release was similarly suppressed by D,L-propranolol (-38 +/- 6% at 0.1 mumol/L, -44 +/- 5% at 1 mumol/L, and -78 +/- 3% at 10 mumol/L) or lidocaine (-39 +/- 7% at 0.1 mumol/L, -58 +/- 9% at 1 mumol/L, and -91 +/- 3% at 10 mumol/L). CONCLUSIONS: These data indicate that propranolol and lidocaine inhibit neural norepinephrine release via a Na+ channel-blocking mechanism that is synergistic with changes induced by ischemia, primarily raised extracellular K+. This mechanism may contribute to the anti-ischemic and antiarrhythmic properties of both agents in acute myocardial ischemia, which induces increased extracellular K+ and sympathetic activation.

Animals↗
PubMed1988

Pindolol, not propranolol, reverses cardiac hypertrophy in renal hypertensive rats.

Reversal of cardiac hypertrophy has been obtained by treatment with some antihypertensive drugs but has not been achieved consistently with beta blockers. To investigate whether this difference might be explained by the distinct hemodynamic actions of the drugs, we studied the effects of propranolol and pindolol, beta blockers with distinct modes of action, on cardiac hypertrophy of hypertensive male Wistar rats, two-kidney, one clip (2K1C) Goldblatt model (n = 33) and sham-operated control rats (n = 34). We also assessed the effects of such therapies on the ventricular pumping ability during open-chest, transient aortic occlusion. Four weeks after surgery, propranolol (5 mg/kg/day p.o.) was given to hypertensive (n = 8) and control rats (n = 11); pindolol was also given orally (1 mg/kg/day) to similar groups (n = 7 and n = 5, respectively). Untreated animals served as controls for both groups. Cardiac hypertrophy developed with hypertension in the untreated rats of the propranolol (3.38 +/- 0.18 vs 2.60 +/- 0.08 mg/g; p less than 0.01) and pindolol groups (3.93 +/- 0.21 vs 2.40 +/- 0.03 mg/g; p less than 0.001). Treatment reversed cardiac hypertrophy in the pindolol-treated (3.01 +/- 0.19 vs 3.93 +/- 0.21 mg/g; p less than 0.001, NS) but not in the propranolol-treated rats (3.24 +/- 0.18 vs 3.38 +/- 0.21 mg/g, NS). The maximal pressure that developed during aortic occlusion in the propranolol group was similar to that observed in the pindolol group. These results indicate that cardiac hypertrophy is reversed by pindolol but not by propranolol, and that this reversal does not interfere with left ventricular pumping ability.

Animals↗
PubMedDate not supplied

Propranolol or hydrochlorothiazide alone for the initial treatment of hypertension. IV. Effect on plasma glucose and glucose tolerance. Veterans Administration Cooperative Study Group on Antihypertensive Agents.

To evaluate the short-term and long-term effectiveness of propranolol and hydrochlorothiazide monotherapy for hypertension, 683 hypertensive men were randomized to treatment with either propranolol or hydrochlorothiazide. Both drugs increased the average fasting plasma glucose level by approximately 5 mg/dl after 10 weeks (p less than 0.001) and 1 year (p less than 0.001) of treatment, but the elevation persisted only in the propranolol-treated group 1 month after discontinuing the year-long treatment (p less than 0.01). A subset of 191 patients had 2-hour glucose tolerance tests. Hydrochlorothiazide increased the average 2-hour oral glucose tolerance test result by 18.0 mg/dl after 10 weeks (p less than 0.001), an increase significantly higher than that induced by propranolol (p less than 0.012). After 1 year of treatment, however, propranolol also increased the average 2-hour oral glucose tolerance test result (p less than 0.05) and there was no significant difference between drugs. The hyperglycemic effects were dose-related, which suggests that both drugs should be administered at their lowest effective dosage. The clinical importance of the persistent fasting plasma glucose elevation in propranolol-treated patients 1 month after discontinuing treatment is unknown.

Adult↗
PubMed1979

Effects of nitroglycerin and propranolol on the distribution of transmural myocardial blood flow during ischemia in the absence of hemodynamic changes in the unanesthetized dog.

Chronically instrumented awake dogs were used to study the effects of nitroglycerin and propranolol on the transmural distribution of myocardial blood flow during transient ischemia. Studies were carried out 7-14 d after implantation of an electromagnetic flowmeter probe and balloon occluder on the left circumflex coronary artery, placement of epicardial minor axis sonar crystals, and implantation of left atrial, left ventricular, and aortic catheters. The occluder was inflated to completely interrupt flow for 10 s followed by partial release to reestablish flow at 60% of the preocclusion level. During this partial release, which served as the control for the study, regional myocardial blood flow was measured with 7- to 10-mum radioactive microspheres. After control measurements, seven dogs were given nitroglycerin (0.4 mg i.v.) and eight dogs propranolol (0.2 mg/kg i.v.). 5 min later the occlusion and partial release sequence was repeated, and regional myocardial blood flow was measured when heart rate, aortic and left ventricular end-diastolic pressure, and minor axis diameter were unchanged from control values.The data values were selected so that total flow to the ischemic region during partial release after nitroglycerin or propranolol administration was not significantly different from flow during the control partial release. After nitroglycerin administration, endocardial flow (endo) in the ischemic region increased from 0.46+/-0.07 to 0.59+/-0.06 ml/min per g (P < 0.006); epicardial flow (epi) decreased from 0.78+/-0.09 to 0.70+/-0.08 ml/min per g (P < 0.04). The endo:epi ratio increased from 0.65+/-0.07 to 0.92+/-0.10 (P < 0.05). In contrast, administration of propranolol produced no significant change in transmural flow (endo, 0.42+/-0.02 and 0.46+/-0.03 ml/min per g; epi, 0.71+/-0.06 and 0.70+/-0.07 ml/min per g) or in the endo:epi ratio (0.60+/-0.03, 0.66+/-0.06) in the ischemic region. Nitroglycerin and propranolol produce different effects on the transmural distribution of blood flow to ischemic myocardium. Nitroglycerin can increase blood flow to the underperfused endocardium in the absence of alterations in heart size, hemodynamic parameters, and total transmural flow to the ischemic region. Under similar conditions, propranolol has no significant effect on the transmural distribution of blood flow to an ischemic region.

Animals↗
PubMed1992

Randomized, double-blind, crossover, placebo-controlled comparison of propranolol and betaxolol in the treatment of neuroleptic-induced akathisia.

OBJECTIVE: Beta-blocking agents, particularly propranolol, are considered effective in the treatment of neuroleptic-induced akathisia, but considerable controversy exists about the involved receptor subtype(s). The authors conducted a randomized, controlled trial comparing the effects of propranolol and betaxolol to determine whether central beta 1-adrenoceptor blockade is sufficient to correct neuroleptic-induced akathisia. METHOD: The subjects were 19 patients whose neuroleptic-induced akathisia responded to 20 mg/day of propranolol and subsequently reemerged during a placebo washout period. They were randomly assigned to propranolol (20 or 40 mg/day) or betaxolol (10 or 20 mg/day) and, after another placebo period, were switched to the second beta blocker. RESULTS: There was no significant difference in the antiakathisia effects of propranolol and betaxolol. CONCLUSIONS: The lack of difference between propranolol and betaxolol suggests that beta 1-adrenoceptor blockade is sufficient to improve neuroleptic-induced akathisia. The results of this explanatory study need therapeutic confirmation.

Adult↗
PubMed1985

Augmentation by propranolol of growth hormone-releasing hormone-(1-44)-NH2-induced growth hormone release in normal short and normal children.

The effect of a 90-min iv infusion of propranolol, a beta-adrenergic antagonist (0.2 mg/kg BW), on basal plasma GH levels and the GH responses to an iv bolus injection of GH-releasing hormone-(1-44)-NH2 (GHRH; 1 microgram/kg BW) was examined in 10 prepubertal children (6 short but otherwise normal and 4 normal). The iv injection of GHRH resulted in significant increases in plasma GH, comparable to those after either insulin-induced hypoglycemia or arginine infusion. Only a small and inconsistent increase in plasma GH levels occurred during the iv infusion of propranolol, whereas simultaneous administration of propranolol with GHRH caused marked enhancement of GHRH-induced GH release in all subjects. The difference between the plasma GH response to GHRH given with propranolol and the response to GHRH given with 0.9% saline was significantly greater than that between the plasma GH level after propranolol and that after 0.9% saline infusion without GHRH injections. There was no difference in plasma GH responses to GHRH, propranolol, or both in the normal short children or normal children. These findings indicate that beta-adrenergic blockade potentiates GHRH-induced GH secretion in prepubertal children.

Child↗