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PubMed1976

Adrenergic inhibition of cell proliferation in the buccal epithelium of rat.

Mitotic rates in the basal layer of cells in the buccal epithelium of rat were measured using a stathmokinetic technique. Adrenaline was found to inhibit cell proliferation in this tissue and the effect of adrenaline could be blocked by the beta-adrenergic antagonist propranolol but not by the alpha-adrenergic antagonist phentolamine nor by the specific beta2-adrenergic antagonist butoxamine. Cell proliferation in the buccal mucosa was also inhibited by terbutaline, a synthetic beta2-adrenergic agonist. The effect of terbutaline was not blocked by either butoxamine or by the specific beta1-adrenergic antagonist practolol.

Animals↗
PubMed2002

Data-mining analyses of pharmacovigilance signals in relation to relevant comparison drugs.

OBJECTIVE: The aim of this paper is to demonstrate the usefulness of the Bayesian Confidence Propagation Neural Network (BCPNN) in the detection of drug-specific and drug-group effects in the database of adverse drug reactions of the World Health Organization Programme for International Drug Monitoring. METHODS: Examples of drug-adverse reaction combinations highlighted by the BCPNN as quantitative associations were selected. The anatomical therapeutic chemical (ATC) group to which the drug belonged was then identified, and the information component (IC) was calculated for this ATC group and the adverse drug reaction (ADR). The IC of the ATC group with the ADR was then compared with the IC of the drug-ADR by plotting the change in IC and its 95% confidence limit over time for both. RESULTS: The chosen examples show that the BCPNN data-mining approach can identify drug-specific as well as group effects. In the known examples that served as test cases, beta-blocking agents other than practolol are not associated with sclerosing peritonitis, but all angiotensin-converting enzyme inhibitors are associated with coughing, as are antihistamines with heart-rhythm disorders and antipsychotics with myocarditis. The recently identified association between antipsychotics and myocarditis remains even after consideration of concomitant medication. CONCLUSION: The BCPNN can be used to improve the ability of a signal detection system to highlight group and drug-specific effects.

Adverse Drug Reaction Reporting Systems↗
PubMed1984

Effects of beta-adrenergic inhibition on scar formation after myocardial infarction.

In view of clinical interest in the efficacy of beta-adrenergic blockade during acute myocardial infarction (AMI), we have determined the long-term effect of therapy on scar formation after experimental myocardial ischemia. Intact anesthetized dogs underwent acute occlusion of the left anterior descending coronary artery, by means of a balloon catheter, which permitted monitoring of the aortic-peripheral coronary artery pressure gradient during the 4-hour period of balloon inflation. Practolol administration was begun 15 minutes after the onset of ischemia in group A. Control animals (group B) received procainamide to approximate the antiarrhythmic action of beta blockade. Only group A exhibited significant reduction in the ST segments during acute ischemia. Chronic therapy was maintained for 1 month and the mature scar formed in the myocardium was assessed after 4 months. The extent of subendocardial scar was similar in both groups but subepicardial scar formation was significantly less in group A. There was also a significant decrease in the percentage of total myocardium involved with scar in this treatment group. Although thinning of the left ventricular wall was similar for both groups in the central scar region, this process was significantly reduced at the lateral margin in group A. Thus, specific beta-receptor blockade during acute myocardial ischemia and sustained during the repair process can result in a reduced quantity and altered distribution of mature scar.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of sulfinpyrazone on ventricular vulnerability in the normal and the ischemic heart.

The effects of sulfinpyrazone were studied in 33 chloralose-anesthetized dogs. Ventricular fibrillation thresholds, mid diastolic thresholds and duration of the effective refractory period were determined in the normal heart after intravenous administration of sulfinpyrazone, 30 mg/kg body weight. The drug significantly raised the ventricular fibrillation threshold by 24 percent and the mid diastolic threshold by 36 percent and prolonged the effective refractory period by seven percent. The influence of sulfinpyrazone during acute myocardial ischemia was evaluated before and during a 10 minute occlusion of the left anterior descending coronary artery and after abrupt release of the occlusion. Although the drug afforded significant protection during coronary occlusion, it had no effect on the ventricular fibrillation threshold after reperfusion. Because potent cardiocardiac reflexes are elicited during ischemia, the influence of sulfinpyrazone on the ventricular fibrillation threshold was studied during norepinephrine infusion. Sulfinpyrazone attenuated the reduction of the ventricular fibrillation threshold during sympathetic humoral stimulation. Its effect was additive to beta adrenergic blockade with practolol and membrane stabilization with lidocaine. This investigation suggests that sulfinpyrazone exerts significant effects on ventricular vulnerability of both the normal and the ischemic myocardium. Further studies are needed to elucidate its precise mechanism of action.

Animals↗
PubMed1983

Chronic beta blockade therapy in patients after myocardial infarction.

This report is a review of greater than 18 years of experience with clinical trials that have examined the effect of beta blockers on mortality after acute myocardial infarction (MI). Despite inadequate sample size, a substantial number of the early randomized trials demonstrated a trend toward reduction in mortality after MI using a number of beta blockers. This review highlights the larger prospective randomized trials, especially the Multicenter International Trial of practolol, the Norwegian Multicenter Study of timolol and the Beta-Blocker Heart Attack Trial (BHAT) of propranolol. The combined strength of these long-term trials, comprising greater than 8,000 patients, demonstrates a consistent and statistically significant reduction in mortality after MI. Both the Norwegian timolol study and BHAT further document a substantial reduction in mortality in patients stratified according to risk groups, with a reduction in mortality after complicated or uncomplicated first MI or in patients with prior MI. These 2 studies also document a reduction in sudden death mortality in the first year after MI. Data regarding subendocardial MI is more variable, but the Norwegian timolol study documents a substantial reduction in mortality after subendocardial MI. Based on this review, we recommend treatment of all patients who can tolerate beta blockade after acute MI, beginning in the late hospitalization phase and continuing for at least 2 years.

Adrenergic beta-Antagonists↗
PubMed1976

Effect of ritodrine on uterine activity, heart rate, and blood pressure in the pregnant sheep: combined use of alpha or beta blockade.

Ritodrine hydrochloride was administered parenterally to pregnant ewes during spontaneous or oxytocin-induced uterine activity. The effects of ritodrine on the uterus and cardiovasculature were assessed both with and without simultaneous administration of either alpha or beta blockade. Ritodrine was found to be an effective inhibitor of both spontaneous and induced uterine activity. Ritodrine did cause maternal tachycardia but no significant hypotension. Alpha-adrenergic blockade did not influence the effects of ritodrine. Beta blockade with propranolol reversed the uterine and cardiovascular effects of ritodrine, whereas beta blockade with practolol reversed the cardiovascular effects without interfering with the inhibition of uterine activity produced by ritodrine.

Adrenergic alpha-Antagonists↗
PubMed1987

Heterogeneity of beta-adrenoreceptors in guinea pig alveolar type II cells.

[3H]Dihydroalprenolol ([3H]DHA) binding to guinea pig alveolar type II cell membrane revealed the presence of both high (KD = 0.38 nM) and low (KD = 4.2 nM) affinity beta-adrenoreceptors. The low affinity site had a higher binding capacity (Bmax = 245.6 fmol/mg protein) than the high affinity site (Bmax = 71.7 fmol/mg protein). Displacement of [3H]DHA by practolol, a selective beta 1 agent, confirmed the existence of two species of adrenoreceptors, corresponding to 21% high affinity (beta 1) and 79% low affinity (beta 2), respectively.

Animals↗
PubMed1981

Subtypes of beta-adrenergic receptors in rat cerebral microvessels.

The 125I-labeled iodohydroxybenzylpindolol (IHYP) binding to beta-receptors on brain micro-vessels is inhibited by isoproterenol, epinephrine and norepinephrine, with Ki values of 2 X 10(-7) M, 2.5 X 10(-6) M and 1.2 X 10(-5) M, respectively. A modified Scatchard analysis of the inhibitory effects of practolol, metroprolol and zinterol on IHYP binding has shown that the proportion of beta 2-receptors in our preparation is about 80% of the total beta-adrenergic receptor population. Our data indicate that the beta-adrenergic receptors located on cerebral microvessels are of both beta 1 and beta 2 types, with a predominance of the beta 2 type.

Animals↗
PubMed1975

Beta-adrenergic blockade and atrio--ventricular conduction impairment.

Atrio--ventricular conduction and its modifications induced by six Beta-adrenergic blocking agents have been investigated in the dog. Premature atrial stimuli (St2) were applied at variable intervals following regular stimuli (St1) ensuring atrial pacing; atrial (AERP), nodoventricular (NERP) and global (GERP) effective refractory periods as well as global functional refractory period (GFRP) were determined before and after administration of each of the six drugs. When Beta-blockade was produced with d,1-propranolol which hwas membrane stabilizing effects (MSE) but no intrinsic sympathomimetic activity (ISA) or with sotalol, which has neither MSE nor ISA, all parameters were significantly increased. When Beta-blockade was achieved with pindolol or practolol, which have only a poor Beta-adrenolytic potency and no ISA. Alprenolol showed intermediate effects. Thus, it appears that Beta-blockade and not MSE, is responsible for the onset of A-V conduction impairment but that ISA, probably through a metabolic mechanism, affords protection against this impairment. On the other hand, measurement of ventricular effective refractory period (VERP) has shown that at the Purkinje-free junction, it is MSE which is mainly involved in conduction impairment.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Antimuscarinic action of an alkane-bis-ammonium compound alone and in combination with (+)-benzetimide.

Heptane-1,7-bis-(dimethyl-3'-phthalimidopropylammonium bromide) ('C7/3-phthalimido-propyl') in concentrations of 10(-7) to 0.5 X 10(-3) inhibited negative inotropic responses to carbachol or acetylcholine to a similar extent in the electrically stimulated isolated guinea-pig left atrium. However, the degree of antagonism of responses to carbachol was less than expected for a competitive antagonist when the higher concentrations of 'C7/3-phthalimido-propyl' were employed. When 'C7/3-phthalimido-propyl' was combined with competitive antagonists such as (+)-benzetimide, atropine or homatropine the degree of antagonism was greater than expected for combination of 2 competitive antagonists. Qualitatively similar results were obtained in the presence of practolol (1.5 X 10(-5) M). The results obtained with 'C7/3-phthalimido-propyl' are shown to agree with theoretical predictions for a metaffinoid antagonist which influences the affinities of both agonists and competitive antagonists by combining with a regulatory site distinct from, but interdependent with the binding sites for agonists and competitive antagonists. Further, it is shown that the alkane-bis-ammonium compound produces a much greater reduction in the affinity of carbachol than that of the competitive antagonists and as a consequence causes 'supra-additive' effects when combined with a competitive antagonist. The reduction in the affinity of (+)-benzetimide produced by 'C7/3-phthalimido-propyl' did not differ significantly from the reduction in the affinities of atropine or homatropine.

Acetylcholine↗
PubMed1975

Effect of propranolol on antinociceptive, tolerance- and dependence-producing properties of morphine in rodents and monkeys.

Since an abstinence syndrome may accompany the injection of opioids in addicts pretreated with propranolol the morphine antagonistic properties of this compound were investigated. Racemic propranolol did not significantly affect the antinociceptive ED50 of morphine in rodents and neither precipitated abstinence in morphine-dependent monkeys nor exacerbated the syndrome in 24 hr withdrawn monkeys. Multiple doses of propranolol did not alter the development of physical dependence on morphine in monkeys. Clinical narcotic antagonism would not be predicted from this profile. Evidence for a possible propranolol-morphine interaction came from studies using the mouse tail flick test. Thus, after 8 injections of propranolol (over 4 days) mice were tolerant to normally effective doses of morphine. Concurrent injections of naloxone antagonised this effect. When propranolol and morphine were administered concurrently the morphine ED50 (on day 5) was twice that of the group receiving morphine alone. Similar results were obtained with d-propranolol; practolol had a neutral effect.

Analgesics, Opioid↗
PubMed1976

Some adrenergic beta-blocking agents affecting lipolysis in human adipose tissue in vitro.

Antagonistic actions of beta-blocking drugs on isoproterenol-induced lipolysis were studied in human omental adipose tissue. Competitive interaciton characterized by the following pA2 values was found: propranolol 8.7; trimepranol 8.7; practolol 7.1; H 35/25 6.0. The plot of pA2 values of these drugs for human versus rat adipose tissue is linear with slope 2.0 indicating a higher differentiation of beta-antagonist actions in human than in rat adipose tissue.

Adipose Tissue↗
PubMed1977

Influence of several anesthetic agents on the effect of delta9-tetrahydrocannabinol on the heart rate and blood pressure of the mongrel dog.

delta9-Tetrahydrocannabinol (delta9-THC) 1 mg/kg, i.v. produced a slight but significant reduction in the heart rate of conscious mongrel dogs, and these effects were greatly potentiated by pentobarbital and/or urethane anesthesia. However, significant increase in the heart rate was noted following delta9-THC administration in the dogs anesthetized with a combination of morphine plus chloralose; further, neither morphine nor chloralose alone could reverse the bradycardic effects of delt9-THC. Tachycardia induced by delta9-THC in these dogs could be reversed by bilateral vagotomy or by pretreatment of the animals with methylatropine, or propranolol and/or practolol. The data indicated a complex interaction between delta9-THC and morphine-chloralose combination and the tachycardia induced by delta9-THC under this anesthesia may be due to release of epinephrine by a reflexogenic mechanism involving afferent vagi. Further, while the bradycardic effects of delta9-THC were essentially identical under pentobarbital or urethane anesthesia, the hypotensive effects were similar in urethane or chloralose anesthetized dogs. The study emphasizes that anesthetic interaction should be taken into consideration while investigating mechanisms of actions of pharmacological agents.

Anesthetics↗
PubMed1978

Analysis of the vasodilator action of alprenolol.

The effect of alprenolol and other beta-adrenoceptor antagonists, including d-isomers, on blood flow in femoral, coronary and mesenteric vascular beds was measured in anesthetized dogs. Under conditions of constant perfusion pressure, intra-arterial injection of beta-adrenoceptor antagonists produced vasodilation. Propranolol and alprenolol were approximately equipotent in coronary and mesenteric beds but alprenolol was significantly more potent in the femoral bed. Practolol was virtually inactive in all beds. The vasodilating potency of d-alprenolol and d-propranolol was not significantly different from that of the respective racemic mixtures. The vasodilator response to alprenolol was not affected by pretreatment with atropine, diphenhydramine or propranolol. In conscious normotensive dogs i.v. injections of d,l- and d-alprenolol produced dose-dependent decreases in blood pressure and increases in heart rate. Under similar conditions, i.v. d,l-propranolol was without effect on either measurement. The results suggest that the hypotensive action of alprenolol in dogs may derive from its vasodilator activity.

Alprenolol↗
PubMed1989

Beta-adrenoceptors in human brain labelled with [3H]dihydroalprenolol and [3H]CGP 12177.

beta-Adrenoceptor binding sites were characterised and quantitated in post-mortem human brain with [3H]dihydroalprenolol ([3H]DHA) and [3H]CGP 12177. In cerebral cortex, isoprenaline and propranolol displaced both radioligands with uniform affinity. Practolol and CGP 20712A (selective beta 1-adrenoceptor antagonists) displaced with high affinity from a greater proportion of sites than ICI 118,551 and IPS 339 (selective beta 2-adrenoceptor antagonists). In cerebellum, propranolol displaced both radioligands with uniform affinity. ICI 118,551 displaced with high affinity from a greater proportion of sites than CGP 20712A. The density of total beta-adrenoceptors (defined with isoprenaline) and of beta 1- and beta 2-adrenoceptors (defined with CGP 20712A and ICI 118,551 respectively) was studied by saturation binding of both radioligands in 13 brain areas. beta-Adrenoceptor density was higher in caudate, putamen and nucleus accumbens (100-120 fmol/mg protein) than cortex (50-70 fmol/mg protein) and densities were lowest in hypothalamus and cerebellum (27-38 fmol/mg protein). The proportion of beta 1-adrenoceptors (as a % of total beta-adrenoceptors) was high in caudate (80%), putamen (80%) and cortex (60-70%) and lower in hippocampus (40%) and cerebellum (30%). Both radioligands labelled a very similar number of beta-adrenoceptors in all brain regions studied.

Adrenergic beta-Antagonists↗
PubMed1984

Beta 2-receptors in the rat anterior pituitary mediate adrenergic stimulation of prolactin release.

As previously shown, the beta-adrenergic agonists isoproterenol, epinephrine and norepinephrine stimulate prolactin (PRL) release from superfused rat anterior pituitary cell aggregates. In order to further characterize the beta-adrenergic response in this tissue preparation, the effects of various beta-adrenergic agents were investigated. The beta 2-agonist, zinterol, stimulated PRL release at concentrations more than 4 orders of magnitude lower than prenalterol, a beta 1-agonist with high potency in rat heart. The order of potency of the antagonists IPS 339 (beta 2), ICI 118.551 (beta 2), propranolol, sotalol, practolol (beta 1), metoprolol (beta 1) and H 35/25 for inhibition of beta-agonist-stimulated PRL release provided additional support for a beta 2-stimulatory effect. beta-Agonists were also capable of stimulating PRL release from superfused intact pituitaries. The beta-adrenergic response desensitized rapidly during prolonged exposure of the aggregates to beta-agonists.

Adrenergic beta-Agonists↗
PubMed1983

Beta-1 adrenergic receptors mediate noradrenergic facilitation of Purkinje cell responses to gamma-aminobutyric acid in cerebellum of rat.

Norepinephrine (NE) may have a major role in modulating the responsiveness of Purkinje cells to the actions of other neurotransmitters in the cerebellum. Specifically, the catecholamine has been shown to enhance inhibitory responses of Purkinje cells to microiontophoretically applied gamma-aminobutyric acid (GABA). This noradrenergic facilitation of GABA has been shown recently to be mediated by beta-adrenergic receptors. The aim of this study was to characterize further the subtype of the beta-receptor involved. The results indicate that practolol, a selective beta-1 blocker, antagonized the NE-induced augmentation of Purkinje cell inhibitory responses to GABA. Zinterol, a selective beta-2 agonist, did not mimic the potentiating effect of NE. Furthermore, the noradrenergic facilitation of GABA-induced inhibition remained unaltered in cerebella subjected to neonatal X-irradiation. This procedure resulted in a decrease in the total cerebellar beta-receptor population yet left unchanged both the number of beta-1 receptors per cerebellum and the radio-resistant Purkinje cells. Together, the data presented here support the hypothesis that the noradrenergic facilitation of GABA-induced inhibition of Purkinje cells is mediated by the activation of cerebellar beta-1 adrenergic receptors located on the Purkinje cells.

Animals↗
PubMed1983

Neuroeffector mechanisms of the defense reaction in the rat.

Electrical stimulation of the dorsal periaqueductal gray matter (DPAG) eliciting flight behavior in awake rats caused an increase in arterial blood pressure (BP), heart rate (HR) and respiration in rats anesthetized with urethane. The hypertension was markedly reduced by 5 mg/kg of intravenously injected hexamethonium or bretylium, virtually abolished by 5 mg/kg of phentolamine and partially antagonized by 0.1 mg/kg of the alpha 1-adrenoceptor blocker, prazosin. The tachycardia induced by DPAG stimulation was partially antagonized by hexamethonium or bretylium and abolished by propranolol (5 mg/kg, IV) or practolol (5 mg/kg, IV), but not affected by N-butylscopolamine (10 mg/kg, IV). Phentolamine increased basal HR and abolished the tachycardic response caused by either brain stimulation or intravenous noradrenaline. Prazosin moderately decreased the response to noradrenaline, but did not affect basal HR or the tachycardia induced by brain stimulation. The increase in respiratory amplitude occurring during brain stimulation was abolished by phentolamine as well as by prazosin, while the increase in respiratory rate was moderately reduced by phentolamine and propranolol. These results demonstrate that the cardiovascular component of the defense reaction of the rat is almost entirely due to a sharp increase in sympathetic tone. They also suggest that the hyperventilation induced by aversive brain stimulation is modulated by central and peripheral adrenergic mechanisms.

Animals↗