Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Propranolol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1979

Propranolol in human plasma and breast milk.

To assess the problem of continuing propranolol therapy in a breast-feeding mother, studies were performed to determine simultaneously plasma and breast milk concentrations of propranolol after single dose (40 mg) and continuous dose (40 mg 4 times daily) treatment with this drug. Breast milk and plasma concentrations of propranolol peaked between 2 and 3 hours after dosing. Propranolol concentrations in breast milk were less than 40 and 64 percent, respectively, of peak plasma propranolol concentrations after single dose and continuous dose administration. It was estimated that the maximal cumulative propranolol load to this breast-feeding infant, consuming 500 ml of whole milk, when the mother received 40 mg of propranolol 4 times daily would be 21 microgram/24 hours. This dose is considerably less than the usual therapeutic dose of propranolol for infants.

Adult↗
PubMed1981

Slow release oxprenolol in angina pectoris: study comparing oxprenolol, once daily, with propranolol, four times daily.

Oxprenolol and propranolol are noncardioselective beta adrenoreceptor blocking agents known to be equally effective in the management of patients with angina pectoris. Both are usually prescribed four times daily. Slow release formulation of oxprenolol administered once daily has been shown to maintain therapeutic effects for 24 hours. In a double-blind crossover study in 23 patients with stable angina pectoris, the effects of 160 mg slow release oxprenolol, administered once daily for 1 month, were compared with those of 40 mg of propranolol given four times daily for a similar period. No adverse effects occurred when patients were switched between treatment schedules. The average number of anginal attacks experienced were 11/month during oxprenolol therapy and 8/month during propranolol therapy (difference not significant). The resting values for heart rate were higher 7 1/2 nd 24 hours after oxprenolol than they were 4 and 12 hours after propranolol (p less than 0.01). The treadmill walking time to the onset of angina and to the development of moderate angina 24 hours after oxprenolol was less than that observed 7 1/2 hours after the drug or 4 and 12 hours after propranolol (p less than 0.01). In contrast, the values for walking time to the onset of angina and to the development of moderate angina at 4 and 12 hours after propranolol were similar. This decreased exercise tolerance 24 hours after oxprenolol was associated with a lesser degree of beta adrenoreceptor blockade than that present after propranolol as documented by higher levels of heart rate (p less than 0.05), systolic blood pressure (p less than 0.05) and rate-pressure product (p less than 0.05) during exercise after oxprenolol therapy. It is concluded that in the doses used, slow release oxprenolol administered once daily does not exert as consistent a beneficial effect on exercise tolerance throughout the dosing schedule as does propranolol given four times daily.

Adult↗
PubMed1984

Effects of timolol and propranolol on inducible sustained ventricular tachyarrhythmias in dogs with subacute myocardial infarction.

Timolol and propranolol reduce the incidence of cardiac death after myocardial infarction (MI). To explore possible mechanisms of this reduction in mortality, the antiarrhythmic effects of these 2 beta blockers were compared in a dog model of inducible sustained ventricular tachycardia (VT) or fibrillation (VF) 4 to 6 days after experimental closed-chest MI. Dogs with inducible VT or VF underwent drug studies with timolol and propranolol; the sequence of drug administration was randomized. Timolol doses were 0.1, 0.3, and 1.0 mg/kg; propranolol doses were 1.0, 3.0 and 10.0 mg/kg. Timolol and propranolol were equally effective in abolishing inducible VT or VF: 77% of instances of inducible VT or VF responded to 1 or both beta blockers. The VF threshold was significantly elevated by both timolol and propranolol; the elevation in the VF threshold was significantly greater in "responders," i.e., dogs in whom VT was prevented by beta blockade (15 +/- 9 vs 8 +/- 9 mA, p less than 0.05). The ventricular effective refractory period was prolonged by both drugs; again, more so in the responders than in the nonresponders (16 +/- 9 vs 8 +/- 14 mA, p less than 0.05). The QTc interval was not significantly affected by either beta blocker. Among the responders, no difference was detected between timolol and propranolol in the extent to which the effective refractory period was prolonged or the VF threshold elevated. However, the highest dose of propranolol decreased the mean blood pressure significantly more than the comparable dose of timolol. In conclusion, timolol and propranolol are equally effective in abolishing inducible VT or VF in the dog after subacute MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise.

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 +/- 0.11 to 0.58 +/- 0.12 (p less than 0.001) and 0.56 +/- 0.14 (p less than 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Nifedipine, but not propranolol, improves left ventricular systolic and diastolic function in patients with hypertension.

The effects of nifedipine and propranolol on cardiac function both at rest and at peak exercise were compared in 22 hypertensive patients whose diastolic blood pressures remained in excess of 95 mm Hg despite diuretic therapy. In this double-blind, placebo-controlled study, left ventricular systolic and diastolic function at rest and at peak exercise during bicycle ergometry was assessed by first-pass radionuclide angiography using the Baird Scinticor before and after treatment with either nifedipine or propranolol. Both agents effectively reduced blood pressure in the supine and upright positions and at peak exercise. Nifedipine was associated with a significant increase in cardiac output and stroke volume at rest and at peak exercise, while propranolol decreased cardiac output at rest and at peak exercise. Systemic vascular resistance decreased with nifedipine treatment at rest and at peak exercise, but increased significantly with propranolol. Nifedipine increased ejection fraction in patients at rest and also increased maximal oxygen consumption at peak exercise, while propranolol decreased maximal oxygen consumption at peak exercise. At rest and at peak exercise, nifedipine increased peak filling rate, but time to peak filling rate was not affected by either drug. The fraction of total diastolic filling at the midpoint of diastole was significantly increased by nifedipine therapy at rest but was not affected by propranolol therapy. Nifedipine significantly decreased atrial filling volume while propranolol had no effect. Propranolol therapy did not result in any improvement in left ventricular function. In contrast, nifedipine improved left ventricular systolic and diastolic function at rest and peak exercise. Future selection of an antihypertensive agent should include consideration of the impact of therapy on left ventricular function.

Adult↗
PubMed1986

Comparison of the effects of prazosin versus propranolol on plasma lipoprotein lipids in patients receiving hemodialysis.

A prospective, crossover study was used to evaluate the effects of prazosin and propranolol on lipid metabolism in 10 hypertensive patients receiving long-term hemodialysis therapy. Adequate blood pressure control was achieved with either agent (mean predialysis blood pressure was 144/77 mm Hg). Total triglyceride levels increased by 27 +/- 4 percent during propranolol therapy but decreased during prazosin therapy by 8 +/- 2 percent (p less than 0.05). These changes were accounted for by a 21 +/- 1.5 percent increase in very-low-density lipoprotein triglyceride during propranolol therapy and a 6 +/- 2 percent decrease in very-low-density lipoprotein triglyceride during prazosin therapy (p less than 0.05). Although no change in total cholesterol occurred with either agent, a significant decrease (19 +/- 1 percent, p less than 0.01) in high-density lipoprotein cholesterol occurred with propranolol therapy and an increase of 16 +/- 4 percent occurred during treatment with prazosin (not significant). The high-density lipoprotein2 cholesterol levels decreased by 22 +/- 4 percent after treatment with propranolol and increased by 4 percent after prazosin therapy. Propranolol reduced high-density lipoprotein3 cholesterol levels by 18 +/- 2 percent, whereas prazosin increased these values by 19 +/- 2 percent (p less than 0.01). These changes were associated with a reduction in tissue lipoprotein lipase activity after propranolol therapy (2.4 +/- 0.3 percent) and an increase after prazosin therapy (2.5 +/- 1 percent, p less than 0.05). These data suggest that treatment with propranolol may be associated with unfavorable changes in the lipid profile that are not observed after treatment with prazosin.

Blood Pressure↗
PubMed1989

Chronic stable angina monotherapy. Nifedipine versus propranolol.

A placebo-controlled, double-blind, crossover study was conducted to determine the effects of nifedipine (60 to 90 mg per day) monotherapy and propranolol (240 mg per day) monotherapy on symptoms, angina threshold, and cardiac function in patients with chronic stable angina. Following a two-week placebo period, patients were randomly assigned to receive either nifedipine or propranolol for a five-week treatment period, after which they crossed over to the alternative regimen. All 21 patients were men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. New York Heart Association functional class improved in patients taking either nifedipine or propranolol, and nitroglycerin consumption decreased with both treatments compared with placebo. Nifedipine significantly delayed the onset of chest pain and 1 mm of ST-segment depression during bicycle exercise; increases with propranolol were smaller and not statistically significant. Nine patients had a preferential clinical response to nifedipine compared with six patients to propranolol; this was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvement in radionuclide ejection fraction at identical work loads. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14 percent (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output. Thus, nifedipine is more effective on several measurements than propranolol when administered as single drug therapy in stable angina and has the advantage of preserving cardiac output during exercise.

Adult↗
PubMed1979

The mechanism of modification by propranolol of the metabolism of phosphatidyl-CMP (CDP-diacylglycerol) and other lipids in the rat pineal gland.

The mechanism underlying the alteration of phospholipid metabolism in rat pineal gland in vitro produced by propranolol and tertiary amine local anesthetics was investigated. 0.1 mM propranolol did not affect either the levels or specific activity of [32P]ATP in glands. In the presence of the drug, the incorporation of cytidine, but not of inorganic phosphate, into phosphatidyl-CMP (CDP-diacylglycerol) was dependent on the cytidine concentration. The incorporation of glycerol into phosphatidyl-CMP, phosphatidylinositol and phosphatidylglycerol was enhanced by propranolol, whereas labeling of phosphatidylcholine was decreased. When both 1 mM propranolol and 1 mM inositol were present, labeling of phosphatidylinositol was further increased, stimulation of phosphatidyl-CMP and phosphatidylglycerol labeling was reduced and incorporation into phosphatidylcholine and triacylglycerol was depressed. The incorporation of [3H]inositol into pineal lipids was also enhanced by propranolol. 10 microM propranolol inhibited rat liver phosphatidic acid phosphohydrolase by 50%, while local anesthetics were less potent in the decreasing order: dibucaine greater than tetracaine greater than lidocaine greater than procaine. The propranolol-induced accumulation of phosphatidyl-CMP was prevented by supplying adequate freely diffusible inositol in the medium. The phosphatidyl-CMP which accumulated was not utilized for the enhanced formation of phosphatidylinositol brought about by norepinephrine. The results indicate that propranolol and local anesthetics redirect pineal phospholipid metabolism in part by inhibition of phosphatidic acid phosphohydrolase.

Adenosine Triphosphate↗
PubMed1986

Selective lysosomal uptake and accumulation of the beta-adrenergic antagonist propranolol in cultured and isolated cell systems.

The beta adrenoreceptor antagonist propranolol is rapidly taken up and accumulated in various cultured cell lines. When incubated in the presence of low concentrations of propranolol (10(-9) M), Hela (non-differentiated epithelia), BC3H1 (smooth muscle) and MDCK (differentiated kidney epithelia) cell cultures take up (t1/2 = 4-10 min) and accumulate the drug such that the intracellular concentration is over 1000 times that in the incubation medium. The release of propranolol from the cells was slower (t1/2 = 22 min) than the rate of uptake but the dissociation was stimulated by the addition of 1 microM propranolol to the external medium (t1/2 = 9 min). Uptake, which is non-stereoselective, is dependent on pH and is inhibited by the lysosomotropic agents, NH4Cl, methylamine and chloroquine. At higher concentrations (greater than 10(6) M), uptake is accompanied by a visual swelling of intracellular acidic vesicles staining with acridine orange. These results suggest that propranolol, a basic amphiphilic amine, is accumulated within the lysosomes of these cells. Uptake was confined to these cultured cell systems with no chloroquine-sensitive propranolol uptake, being found in isolated rabbit ventricular myocytes, red blood cells or blood platelets. Although alprenolol and cyanopindolol competed with propranolol for uptake, isoprenaline, adrenaline, noradrenaline, phenylephrine, atenolol, practolol and salbutamol were not effective inhibitors. The possible consequences of this uptake and accumulation of propranolol by certain tissues is discussed in relation to the known actions of the drug, particularly during or after abrupt withdrawal from chronic applications.

Animals↗
PubMed1993

Substrate stereoselectivity and enantiomer/enantiomer interaction in propranolol metabolism in rat liver microsomes.

The substrate stereoselectivity and enantiomer/enantiomer interaction of (S)- and (R)- propranolol for the formation of their metabolites were investigated in rat liver microsomal fractions. The enantiomers of primary metabolites of propranolol, 4-, 5-, 7-hydroxy- and N-desisopropyl-propranolol were separated and assayed by an HPLC method employing a chiral ovomucoid column. Regioselective substrate stereoselectivity (R < S for 4- and 5-hydroxylations; R > S for 7-hydroxylation; R = S for N-desisopropylation) was observed in the formation of propranolol metabolites when the individual enantiomers or a racemic mixture of propranolol were used as substrates. Concentration-dependent metabolic inhibition of propranolol enantiomers by their optical isomers was also observed. In addition, the inhibition of propranolol 4-, 5- and 7-hydroxylations between the enantiomers showed a typical competitive nature. These findings suggested that the propranolol enantiomers competed for the same enzyme, probably a cytochrome P450 isozyme in the CYP2D subfamily.

Animals↗
PubMed1994

Sphingosine-like stimulatory effects of propranolol on phospholipase D activity in NIH 3T3 fibroblasts.

Propranolol and sphingosine exhibit several common biochemical effects, including inhibition of phosphatidic acid phosphohydrolase and protein kinase C (PKC) activities. In NIH 3T3 fibroblasts, sphingosine has also been shown to stimulate phospholipase D (PLD)-mediated hydrolysis of both phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) (Kiss Z and Anderson WB, J Biol Chem 265: 7345-7350, 1990). The present study demonstrates that in [14C]palmitic acid-labeled NIH 3T3 fibroblasts, propranolol (50-100 microM) and sphingosine had similar stimulatory effects on PLD-mediated synthesis of phosphatidylethanol in the presence of ethanol. In [14C]choline- and [14C]-ethanolamine-labeled fibroblasts, both compounds also stimulated the hydrolysis of both [14C]PtdCho and [14C]PtdEtn. However, while sphingosine preferentially stimulated PtdEtn hydrolysis, propranolol had greater effects on PtdCho hydrolysis. At each time point examined (15-45 min), lower concentrations (25-50 microM) of propranolol and 100 nM phorbol 12-myristate 13-acetate (PMA) synergistically enhanced PtdEtn hydrolysis; a higher concentration (100 microM) of propranolol inhibited this PMA effect only when the incubation time was 45 min. On the other hand, propranolol (10-100 microM) had either no effect or it inhibited PMA-induced PtdCho hydrolysis after treatments for 15 or 45 min, respectively. These potentiating and inhibitory actions of propranolol on the hydrolysis of PtdCho and PtdEtn were similarly elicited by sphingosine. The present study identified the PLD system as another common target for the pharmacological actions of sphingosine and propranolol.

3T3 Cells↗
PubMed1994

Role of the CYP2D subfamily in metabolism-dependent covalent binding of propranolol to liver microsomal protein in rats.

In vitro covalent binding of a chemically reactive metabolite of propranolol to microsomal macromolecules, which is presumed to cause inhibition of its own metabolism in rats, was diminished in liver microsomes from rats pretreated with propranolol. Covalent binding was suppressed by the addition of an antibody against P450BTL, which is a cytochrome P450 (P450) isozyme belonging to the CYP2D subfamily. SDS-PAGE of microsomal proteins after incubation with [3H]propranolol and NADPH indicated that the binding was non-selective but prominent at the molecular mass of approx. 50 kDa, corresponding to those of the P450 protein. The radioactivity peak was markedly but not completely diminished by the addition of reduced glutathione. In a reconstituted system containing P450BTL, NADPH-cytochrome P450 reductase (fp2) and dilauroylphosphatidylcholine, propranolol 4-, 5- and 7-hydroxylase activities decreased time dependently following preincubation with propranolol in the presence of NADPH, indicating time-dependent inactivation of P450BTL. The covalent binding of a reactive metabolite of [3H]propranolol to the proteins was also observed in this system. SDS-PAGE showed that among the three proteins in the reconstituted system, fp2 and P450BTL consisting of two polypeptides with molecular masses of 49 and 32 kDa, the binding was specific for a polypeptide corresponding to the P450 isozyme with a molecular mass of 49 kDa. In addition, the ratio of the amount of covalently bound radiolabelled materials to that of P450BTL which was estimated from each impaired propranolol hydroxylase activity under the same reconstitutional conditions was calculated to be approx. 1.0. These findings indicate that propranolol is a mechanism-based inactivator of a cytochrome P450 isozyme(s) belonging to the CYP2D subfamily.

Amino Acid Sequence↗
PubMed1995

Propranolol disposition in Chinese subjects of different CYP2D6 genotypes.

Propranolol pharmacokinetics among different genotypes of CYP2D6 was compared in this study. The Chinese (Han) population consisted of 44 healthy unrelated individuals living in southern Taiwan. Endonuclease tests based on polymerase chain reaction were used to determine C/T188 genotypes of CYP2D6 in leukocyte deoxyribonucleic acid. Based on codon 188 genotypes, subjects were categorized into three groups: homozygous C/C188 (n = 13), heterozygous C/T188 (n = 14); and homozygous T/T188 (n = 17). Each subject was given a 40 mg propranolol tablet. Blood samples were drawn before and 12 hours after propranolol administration to measure propranolol and 4-hydroxypropranolol. Three genotypes showed distinct time profiles of plasma propranolol and 4-hydroxypropranolol. The area under plasma concentration curve values (mean +/- SEM), were 322.0 +/- 40.8, 481.6 +/- 77.5, and 766.1 +/- 92.8 nmol.hr/L, respectively, for C/C188, C/T188, and T/T188 subjects (p < 0.05). The 48-hour excreted amount of 4-hydroxy-S-propranolol-O-glucuronide, but not 4-hydroxy-R-propranolol-O-glucuronide, was significantly higher for C/C188 than for T/T188 subjects (p < 0.05). This study shows a different propranolol disposition in Chinese subjects of different CYP2D6 genotypes.

Adrenergic beta-Antagonists↗
PubMed1979

An opposing role for the adrenals in the hypotensive effects of propranolol in the spontaneously hypertensive rat.

d,l-Propranolol (1 and 5 mg/kg s.c.) did not cause a fall in blood pressure and induced only a limited decrease in heart rate in conscious spontaneously) hypertensive rats (SHR). In contrast, after bilateral adrenalectomy, d,l-propranolol induced a rapid and profound decrease in blood pressure and heart rate. Decreases in heart rate and blood pressure in the individual animals were not correlated. The effects were mainly caused by l-propranolol but an additional effect of d-propranolol cannot be excluded. The decrease in blood pressure was not observed after removal of the adrenal medulla. Heart rate decreased only slightly in these animals. After treatment of adrenalectomized SHR with corticosterone (1 mg/kg b.w./h) the decrease in blood pressure due to d,l-propranolol was completely abolished. The fall in heart rate was diminished. Central injection of d,l-propranolol into the lateral brain ventricle of adrenalectomized SHR caused cardiovascular changes which were less pronounced than those following peripheral injection of comparable doses. The inhibitory effects of d,l-propranolol also occurred in adrenalectomized normotensive Wistar Kyoto rats. However, no significant changes in blood pressure and only a limited fall in heart rate were observed in adrenalectomized normotensive and renal hypertensive Wistar rats. It is concluded that the presence of the adrenal cortex, but not of the adrenal medulla prevents acute hypotension and bradycardia after propranolol in the conscious SHR.

Adrenal Glands↗
PubMed1990

Reversal of alpha-adrenoceptor blockade by propranolol in isolated rat pulmonary artery.

Pulmonary artery rings were prepared from rats (group I to VI, n = 5-7 per group) in order to investigate if a beta-adrenoceptor antagonist interferes with the effect of alpha-adrenoceptor blockade. In I, four cumulative noradrenaline (NA) dose-response curves (10(-9) to 10(-3) M) were constructed. In II, NA curves were constructed first, without blockers, then in the presence of phentolamine (10(-6) M), then propranolol (10(-8) M), then phentolamine plus propranolol (10(-8) M). III, IV and V were treated similar to II, except that atenolol (10(-8) M), ICI 118,551 (10(-8) M) and propranolol (10(-6) M), respectively, were added instead of propranolol (10(-8) M). In VI, NA (10(-6) M) was added followed by phentolamine and then propranolol (10(-9) to 10(-6) M). Phentolamine shifted the NA curve to the right with an increase in the EC50 value. Propranolol but not atenolol or ICI 118,551, reduced the elevated EC50 values caused by phentolamine. In group VI, the increase in force by NA was reduced by phentolamine; the effect of phentolamine was completely abolished by propranolol. Thus, propranolol interferes with the effect of phentolamine in the rat pulmonary artery.

Adrenergic alpha-Antagonists↗
PubMed1991

Enhancement of post-hypoxic contractile and metabolic recovery of perfused rat hearts by dl-propranolol: possible involvement of non-beta-receptor mediated activity.

The present study was undertaken to elucidate a possible role of non-beta-receptor mediated effects in dl-propranolol-induced enhancement of post-hypoxic contractile and metabolic recovery in perfused rat hearts. The rat hearts were perfused for 30 min under reoxygenated conditions following 15 min-substrate free-hypoxic perfusion, and the cardiac performance and myocardial metabolism were examined. Hypoxia induced complete cessation of cardiac contractile force, depletion of myocardial high-energy phosphates, release of ATP metabolites and creatine kinase from the heart. Subsequent reoxygenation produced little recovery of cardiac contractile activity and tissue high-energy phosphates, further enhancement of the release of creatine kinase and the accumulation of tissue calcium. Treatment of the hypoxic hearts with dl-propranolol, d-propranolol and atenolol was performed during 5 to 15 min of hypoxic perfusion. dl-Propranolol and d-propranolol at the concentration of 45 microM elicited a significant recovery of cardiac contractile activity and restoration of myocardial high-energy phosphates. This treatment also resulted in a suppression of the release of creatine kinase and ATP metabolites and the tissue calcium accumulation observed during hypoxia and/or reoxygenation. However, such beneficial effects were not seen in hearts treated with 45 microM atenolol. dl-Propranolol and atenolol, but not d-propranolol, in a concentration of 45 microM have been shown to reveal beta-adrenoceptor blocking action. Thus, the results suggest the involvement of non-beta-receptor mediated effects of propranolol in the enhanced post-hypoxic contractile and metabolic recovery of the perfused rat heart. The non-beta-receptor mediated activity of these drugs appears to be related to their ability to suppress the maximal driving frequency of left atrial preparations.

Animals↗
PubMed1984

Reduction of increased levels of blood glycerol and ketone bodies by propranolol in human hyperthyroidism: role of the fall of the triiodothyronine level.

Hyperthyroid patients in the postabsorptive state have elevated levels of blood glycerol and ketone bodies (KB): this is believed to be due to increased lipolysis and ketogenesis. These increased glycerol and KB levels return toward normal after oral propranolol administration. In order to investigate the mechanism of action of propranolol in hyperthyroid patients, we compared the effects of the oral administration of propranolol with those of timolol, propylthiouracil (PTU), and a placebo. The placebo had no effect. The free thyroxine index, immunoreactive insulin level and glucagon level were not modified by propranolol, timolol, or PTU. Propranolol decreased the pulse rate (P less than 0.01) and the levels of serum triiodothyronine (T3; P less than 0.05), blood glycerol (P less than 0.01), and KB (P less than 0.01). Like propranolol, timolol decreased the pulse rate (P less than 0.01) but had no effect on the T3, glycerol, or KB levels. Propylthiouracil did not modify the pulse rate, but like propranolol, it decreased the T3 (P less than 0.05), glycerol (P less than 0.01) and KB (P less than 0.01) levels. These results suggest that the metabolic actions of propranolol are not caused by its hemodynamic effects nor its beta-blocking properties but are mediated by the decrease of the T3 level.

Adolescent↗
PubMed1992

Effects of acute and subchronic administration of propranolol on the social behaviour of mice; an ethopharmacological study.

The effects of dl-propranolol on the behaviour of adult male CD1 mice were examined after acute intraperitoneal injection (1.5 and 6 mg/kg) and after administration for 10-13 days in the drinking fluid at 12.4 mg/l (1.9 mg/kg daily) and 24.9 mg/l (4.6 mg/kg daily). The behaviour of each mouse was examined by ethological procedures during 5 min social encounters with an untreated partner in an aversive and a less aversive situation, an unfamiliar neutral cage and the animals' home cage. The behaviour of each mouse also was monitored for 5 min in the light-dark box. In the acute studies, behavioural observations commenced at 30 min after the injection. In the light-dark box, propranolol, after acute administration, increased the number of transitions between the light and dark compartments and increased scanning in the light area but propranolol had no significant effect after subchronic administration. In the home cage, propranolol significantly increased social investigation during social encounters and reduced exploratory activity at all doses tested, after both acute and subchronic administration. In the neutral cage, propranolol, after acute administration, increased digging of the sawdust and decreased exploratory activity at both dose levels, while at the largest dose it also increased social investigation. In the neutral cage, propranolol, given by subchronic administration, increased aggressive behaviour as well as social investigation and digging of the sawdust at both dose levels, while reducing non-social exploratory activity. The largest dose of propranolol also increased investigation of the substrate. These results indicate that propranolol increased reactivity to normal environmental and social stimuli, in addition to its anxiolytic profile of behavioural effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aggression↗