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At least 649 records · Page 36Linked to original sources
PubMed1978

Vasodilatation and modulation of vasoconstriction in canine subcutaneous adipose tissue caused by activation of beta-adrenoceptors.

The present experiments were undertaken to study the balance between vascular alpha- and beta-adrenoceptors in canine subcutaneous adipose tissue during sympathetic nerve stimulation and noradrenaline injections. Propranolol potentiated and prolonged the vasoconstrictor response to close i.a. injections of noradrenaline. The vasoconstriction induced by brief nerve stimulation (0.5 to 8 Hz) was, however, unaltered by the beta-adrenoceptor blockade. During prolonged nerve stimulation the vasoconstrictor response was well maintained at 1.5 Hz but at 4 Hz there was a gradual escape. The escape phenomenon at 4 Hz was diminished by propranolol. The beta1-selective antagonist practolol, like propranolol, potentiated and prolonged the vasoconstriction induced by noradrenaline injections and reduced the vasoconstrictor escape during prolonged nerve stimulation at 4 Hz. Furthermore, the vasodilatation induced by noradrenaline injection or nerve stimulation during alpha-adrenoceptor blockade was diminished by practolol. Practolol also blocked the lipolytic response to noradrenaline and nerve stimulation. The beta2-selective antagonist H35/25 blocked the effects of the beta2-selective agonist salbutamol but failed to alter noradrenaline as well as nerve stimulation induced vascular and lipolytic beta-adrenoceptor responses. The present results provide further support for the hypothesis that vascular beta-adrenoceptors in adipose tissue are humoral (noninnervated), preferentially activated by circulating noradrenaline. Moreover, both vascular and lipolytic beta-adrenoceptors activated by noradrenaline in adipose tissue are best classified as beta1-adrenoceptors.

Adipose Tissue↗
PubMed1974

New approach to assessment of cardioselectivity of beta-blocking drugs.

Propranolol, practolol, and placebo were each given intravenously at weekly intervals to six normal subjects, and their effects on respiratory function tests and heart rates assessed. The reduction in the exercise heart rate after each of the two drugs was most comparable at six hours, indicating a similar degree of cardiac beta-blockade, when the plasma concentration ratio of practolol to propranolol was 28:1. The peak flow rate (PFR) was higher at all times during exercise than at rest. There were significant differences between the changes in resting and exercise PFR after placebo and the reductions after propranolol (except at 24 hours), but not after practolol-and the latter's influence on PFR seemed to be intermediate to that of propranolol and placebo. At six hours, when the cardiac beta-blocking activity of the two drugs was almost the same, there was a significant difference (P 0.025) between the reductions in exercise PFR associated with each drug.

Adult↗
PubMed1975

Treatment of spontaneous angina pectoris with beta blocking agents. A clinical, electrocardiographic, and haemodynamic appraisal.

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.

Angina Pectoris↗
PubMed1989

Intracoronary injections of salbutamol demonstrate the presence of functional beta 2-adrenoceptors in the human heart.

To demonstrate the presence of functional cardiac beta 2-adrenoceptors in man, we studied the responses to intracoronary injections of salbutamol in three groups of six patients. We injected salbutamol, a selective beta 2-adrenoceptor agonist, into the right coronary artery to avoid peripheral vasodilator action and to stimulate the sinoatrial node directly. Salbutamol injections caused a sinus tachycardia. The same doses of salbutamol injected into the aortic root caused no change in heart rate, ruling out a systemic effect. The mean dose required to cause an increase in heart rate of 30 beats/min (IHR30) was 2.6 micrograms in the first group of six patients. In 12 other patients salbutamol was given after beta-blockade to confirm the beta 2-selectivity of the responses. Doses of practolol (beta 1-selective blockade) and of propranolol (beta 1- and beta 2-blockade) that had equal beta 1-blocking activity were used. In six patients who were given practolol, the mean IHR30 dose was 2.1 micrograms. In six patients who were given propranolol, the mean IHR30 dose was significantly greater at 64 micrograms (p less than 0.001, practolol vs. propranolol). This study demonstrates that direct cardiac beta 2-adrenoceptor stimulation in man has a positive chronotropic effect.

Albuterol↗
PubMed1977

Beta-adrenergic blockade as adjunctive oral therapy in patients with chronic atrial fibrillation.

In many patients with chronic atrial fibrillation, it is difficult to prevent an excessive ventricular rate under stress, even with high levels of digoxin in the blood. The effect of adding beta-adrenergic blockade with practolol to digoxin on the heart rate at rest and during low-grade controlled exercise was investigated in 28 patients with chronic atrial fibrillation and in ten normal control subjects who were receiving maintenance dosages (0.25 to 0.75 mg) of digoxin. In atrial fibrillation, therapy with practolol decreased the mean heart rate at rest from 99.8 beats per minute to 77.5 beats per minute (23 percent reduction; P less than 0.01) and during mild exercise from 148.9 beats per minute to 105.4 beats per minute (29 percent) reduction (P less than 0.001). Fifteen patients had clinically significant heart failure; therapy with practolol did not worsen it. Reversible side effects were detected in two patients. When therapy with digoxin is not sufficient to control atrial fibrillation, the addition of a beta-adrenergic blocking agent is recommended as adjunctive treatment in selected patients.

Administration, Oral↗
PubMed1979

Effect of two types of beta-adrenergic blockade on gastric acid secretion during pentagastrin stimulation in non-vagotomized and in vagotomized gastric fistula dogs.

The effect of beta-adrenoceptor blockade by propranolol and practolol on submaximally pentagastrin-stimulated gastric acid secretion was studied in conscious non-vagotomized and in vagotomized gastric fistula dogs. Propranolol (0.5 mg/kg) intravenously augmented gastric acid output in vagotomized dogs, more after truncal and selective vagotomy than after parietal cell vagotomy. Vagally innervated dogs also showed an increase, but to a lesser degree and not statistically significant. The increase restored the acid output to preoperative levels in the vagotomized dogs. Practolol (1.0 mg/kg) intravenously resulted in a slight and insignificant increase in acid output in dogs with truncal vagotomy and had only a negligible effect in vagally innervated dogs and after selective and parietal cell vagotomy. It is concluded that propranolol augments pentagastrin-stimulated acid output in vagotomized dogs, and this augmentation was most pronounced in the totally vagotomized stomach. Practolol had minor influence on gastric acid secretion. This effect of the two beta-blocking agents indicates that beta 2-blockade is most important for the secretory augmentation. The restoration of postvagotomy acid secretion to preoperative levels suggests that adrenergic influence is important for the decrease in pentagastrin-stimulated acid secretion after vagotomy.

Adrenergic beta-Antagonists↗
PubMed1983

The effect of alpha- and beta-adrenergic agonists and blockers on postprandial pancreatic polypeptide release in dogs.

The influence of adrenergic agonists--phenylephrine (alpha), isoproterenol (beta), and salbutamol (beta 2)--and of adrenergic blockers--phentolamine (alpha), pranolol (beta), and practolol (beta 1)--on the postprandial pancreatic polypeptide (PP) release has been assessed in five Labrador retrievers. Infusions of phenylephrine, 0.12 mg kg-1h-1; isoproterenol, 3 micrograms kg-1h-1; salbutamol, 12 micrograms kg-1h-1, did not significantly affect PP release. Propranolol, 0.5 mg kg-1, and propranolol, 0.5 mg kg-1, + phentolamine, 1 mg kg-1, combined, given as intravenous boluses before the meal significantly reduce PP release (44% and 58% of controls, p less than 0.05), whereas phentolamine, 1 mg kg-1, and practolol, 1 mg kg-1, had no effect. Phenylephrine combined with phentolamine and isoproterenol combined with propranolol and practolol did not influence PP secretion. It is concluded that the postprandial PP release is stimulated by beta 2-adrenergic mechanisms.

Adrenergic alpha-Agonists↗
PubMed1976

On the beta-adrenergic contribution to the gastric acid and gastrin responses to hypoglycaemia in man.

To study the beta-adrenergic contribution to the hypoglycaemic stimulation of gastric acid and gastrin release the effect of an equal and extensive beta-adrenergic blockade with three drugs was studied. Propranolol was investigated in 12, pindolol in 22, and practolol in 11 patients. Fasting concentration of gastrin serum and spontaneous acid secretion were not reduced by the drugs. Propranolol eliminated the gastrin response to hypoglycaemia, pindolol reduced it, and practolol caused no alteration. The hypoglycaemic acid response was reduced by all three drugs, propranolol reduced the response to one-half and was the strongest inhibitor, practolol the weakest. It is concluded that beta-adrenergic receptors may be of major importance for the hypoglycaemic stimulation of the stomach, but the receptors respond differently from the receptors in the heart.

Adult↗
PubMed1991

A comparison of the inotropic effects of dopamine and epinine in human isolated cardiac preparations.

The positive inotropic effects of epinine and dopamine have been studied in isolated preparations obtained from human heart in the absence and in the presence of the selective beta adrenoceptors antagonists practolol and ICI 118,551. ED50 values of the two agonists were similar (about 3 x 10(-5) M). The inotropic efficacy of epinine was significantly higher than that of dopamine in adult ventricular and papillary muscles, it was similar to that of dopamine in juvenile myocardial preparations and in adult atria and pectinate muscles. The dopamine-evoked response was significantly more sensitive to practolol than epinine-evoked response, but it was less sensitive to ICI 118,551. pA2 values of practolol and ICI 118,551 were considerably different with epinine but not with dopamine as agonist. The results indicate that, compared to dopamine in isolated human heart preparations, epinine was more potent at beta-2 relative to beta-1 adrenoceptors.

Deoxyepinephrine↗
PubMed1979

Transmission blockade and stimulation of ganglionic adenylate cyclase by catecholamines.

Isolated rat superior cervical ganglia treated with isoproterenol and related drugs show an increase in ganglionic cyclic adenosine 3':5'-monophosphate (cAMP) and a block of transmission. For isoproterenol, the maximum increase in cAMP occurred at 1 X 10(-6) M, a concentration without effect on transmission. Approximately 5 X 10(-4) M isoproterenol was required to reduce the ganglionic compound action potential by 50%. Dopamine, in contrast to isoproterenol, had no effect on the content of cAMP but depressed transmission. The maximum increase in cAMP produced by norepinephrine occurred with 5 X 10(-4) M, a concentration that reduced transmission by approximately 35%. The effects of isoproterenol on adenylate cyclase and transmission were prevented either by practolol (10(-4) M) or phentolamine (10(-5) M). Dopamine-induced blockade of transmission was antagonized by phentolamine (10(-5) M). Whereas the blockade of transmission by norepinephrine was antagonized by practolol (10(-5) M) or phentolamine (10(-5) M), the stimulation of adenylate cyclase by norepinephrine was prevented by practolol (10(-4) M) but not by phentolamine (10(-5) M). These results show that the blockade of transmission and stimulation of adenylate cyclase are unrelated in rat ganglia and that adrenergic receptor classification is ambiguous. The role of adenylate cyclase in ganglia is unclear.

Adenylyl Cyclases↗
PubMed1975

Effects of beta adrenergic blocking agents on erythropoietin production in rabbits exposed to hypoxia.

The effects of dl-propranolol, d-propranolol, butoxamine or practolol on erythropoietin (ESF) production in rabbits exposed to hypoxia (0.42 atmosphere) for 18 hours were investigated. Rabbits treated with dl-propranolol (4 or 8 mg/kg i.p.) or butoxamine (15 or 30 mg/kg i.p.) produced significantly less ESF in response to hypoxia than did saline-treated control animals. ESF production in rabbits given d-propranolol or practolol during hypoxia was not significantly different from that of control animals exposed to hypoxia. Based on the proposed selectivity of butoxamine for beta2 adrenergic receptors and of practolol for beta1 adrenergic receptors, it is suggested that ESF production in rabbits exposed to hypoxia may involve the activation of beta2 adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1975

Effect of beta-adrenoceptor blocking drugs, physostigmine, and atropine on the toxicity of doxepin in mice.

Large doses of doxepin given intravenously to animals cause tachyarrhythmias, and still higher doses lead to a progressive and, finally, lethal bradycardia. The effect of pretreatment with five different beta-adrenoceptor blocking drugs (propranolol, alprenolol, practolol, metoprolol or tolamolol), p physostigmine, or atropine on these toxic actions of doxepin was investigated. Mice were sedated with diazepam. Doxepin was injected i.v. 0.1 mg every 15 sec until death. ECG was recorded at 10 sec after every injection. All five beta-blockers injected i.p. 30 min before doxepin inhibited the doxepin-induced tachyarrhythmias. None of the drugs prevented or postponed the death of mice. Large doses of beta-blockers dose-dependently enhanced the doxepin-induced bradycardia and accelerated death. The cardioselective beta-blocking drugs practolol and metoprolol proved less active in enhancing bradycardia than the third cardio-selective drug, tolamolol, and non-selective propranolol and alprenolol. This difference may have resulted from properties other than beta-blockade since practolol and metoprolol lack the "cardiodepressant" and local anaesthetic properties. Since physostigmine and atropine did not modify the doxepin effects the anticholinergic property may not be important in the severe cardiotoxic effects of doxepin.

Adrenergic beta-Antagonists↗
PubMed1978

Beta adrenergic blockade, regional left ventricular blood flow and ST-segment elevation in canine experimental myocardial ischemia.

The effects of dl-propranolol, d-propranolol, dl-pindolol and dl-practolol on regional myocardial blood flow (assessed by means of tracer microspheres) and on ST-segment elevation in ischemic and nonischemic areas of the canine left ventricle have been investigated. dl-Propranolol and dl-pindolol, but not dl-practolol and d-propranolol, induced blood flow redistribution from the epicardium to the endocardium both in ischemic and nonischemic areas. dl-Propranolol-induced redistribution was abolished by atrial pacing at the control heart rate value. These results indicate that the redistribution phenomenon only occurs if both a bradycardia-inducing beta1 adrenoreceptor blockade and a coronary vessels beta2 adrenoceptor blockade are simultaneously achieved. All four drugs significantly decreased ST-segment elevation in ischemic areas. Under atrial pacing, this effect was abolished with dl-practolol but only reduced with dl- and d-propranol, suggesting that, besides bradycardia, membrane stabilization might be involved in protection against ST-segment elevation in ischemic areas.

Adrenergic beta-Antagonists↗
PubMed1978

Effect of beta-sympatholytic agents on vascular responses to noradrenaline and potassium chloride.

Vasoconstrictory responses to noradrenaline (NA) or high potassium chloride (130 mM) usually show a biphasic behaviour: an initial peak is followed by a lower steady state level. The influence of three beta-sympatholytic agents (propranolol, pindolol, practolol) and a "Ca-antagonist" (verapamil) on this particular behaviour of KCl-induced vasoconstrictions was compared with responses to NA. Studies were performed on the intact vascular bed of an isolated intestinal preparation of the rat. 1. Increases in the concentration of propranolol and pindolol from 10(-10) to 10(-6) M attenuated the vascular responses to high KCl. Practolol, however, distinctly enhanced the KCl-responses. NA (1.3 microgram/ml)-elicited vasoconstriction was found to be influenced in a similar manner by the beta-receptor antagonists used, though lower concentrations of pindolol had an enhancing, higher concentrations a reducing effect on the constrictory responses to NA. 2. The extent to which the biphasic response adjusted to the steady state level was concentration-dependently increased KCl-responses and significantly decreased to a monophasic response to NA, in the presence of the beta-sympatholytic agents. 3. By using a quotient of deltaPs (steady-state phase) to deltaPi (initial vasoconstriction) and by comparing the effect of the three beta-sympatholytic agents with that of verapamil on this quotient showed a concentration-dependent decrease in presence of the beta-sympatholytic as well as of the Ca-antagonistic agents. These myotropic actions, i.e. negative influences on the mechanism of vascular smooth muscle activation ranged in the following sequence: Verapamil greater than propranolol greater than pindolol greater than practolol. 4. The mechanism underlying the biphasic responses to high potassium chloride are concluded to be basically different from the NA-responses because they are inversely affected by beta-sympatholytic agents. The steady-state response to KCl was found to be very sensitive to non-specific pharmacological actions of beta-sympatholytic substances. The myotropic action of the beta-receptor antagonists is compared with that of the Ca-antagonist verapamil and the role of calcium in the mechanism of activation of vascular smooth muscle is discussed.

Adrenergic beta-Antagonists↗
PubMed1978

Radioiodinated derivatives of beta adrenoceptor blockers for myocardial imaging.

Four new beta-adrenoceptor blocking agents carrying tyramine as the amino moiety were synthesized and the distribution of their I-125-tagged derivatives evaluated in rats. This distribution was compared with the distribution of various agonists and antagonists labeled with H-3 and C-14, and with the in vitro binding affinity of the new derivatives. A radioiodinated derivative of a cardioselective blocker, alprenolol, showed poor blood clearance and no cardiac selectivity. A derivative of another cardioselective blocker, practolol, showed a promising heart-to-blood ratio (ca. 19) and cardioselectivity with a heart-to-lung ratio of ca. 2. Two additional practolol analogs showed no improvement over the practolol derivative; because of the increased lipophilicity of these derivatives, blood clearance and cardioselectivity were diminished. An inverse correlation is suggested between the dissociation constant for the beta adrenoceptor in the lung and the heart-to-blood and heart-to-lung values. We conclude that polarity plays an important role in the blood clearance and cardioselectivity of these beta-adrenoceptor derivatives.

Adrenergic beta-Antagonists↗
PubMed1988

The correlation between CK MB curve type and the clinical course of recent myocardial infarction.

In 265 patients with acute myocardial infarction (MI) for whom the 72-hour CK MB curve was obtained, three types of a curve were found: with a single and early 16 h peak value (type A), with a single late 16 h peak value (type B), and with a double peak (type C). Type A of the CK MB curve was found in 32% of patients with acute MI, type B in 55% and type C in 13%. There were no significant differences of CK MB max between the type groups. Infarct size differed significantly between groups (A-29 +/- 19, B-35 +/- 22, C-53 +/- 30 g Eq CK MB). In-hospital mortality also differed significantly particularly between type C (31%) and type A groups (5%). Nitroglycerin or practolol given intravenously during the first 48 hours changed the CK MB curve mainly by decreasing CK MB max as compared to controls treated conventionally. There was no effect of treatment with either nitroglycerin or practolol on the clinical course in patients with type A CK MB curve. There is a good correlation between the CK MB curve type and the clinical course of MI. Nitroglycerin or practolol decreased the infarct size only in patients with either B or C type of CK MB curve, having no influence in patients with a mild form of acute MI (type A).

Adult↗
PubMed1984

The effect of sympathomimetic agents on gastric acid secretion in rats.

Beta-adrenoceptor agonists have been reported to inhibit gastric acid secretion in vivo but their site and mode of action is uncertain. A study of the effects of such agents on acid secretion in the rat has been made using both an in vivo preparation and an in vitro one where possible effects due to neural, hormonal or cardiovascular actions of beta-agonists are avoided. In conscious rats with Heidenhain pouches, isoprenaline (40 micrograms kg-1h-1) inhibited the response to pentagastrin (20 micrograms kg-1h-1). This inhibition was abolished by propranolol (2 mg kg-1) and butoxamine (8 mg kg-1) and partially reversed by practolol (8 mg kg-1). Propranolol alone (2 mg kg-1) significantly increased the response to pentagastrin in the pouch rats but butoxamine and practolol (both at 8 mg kg-1) and the inactive isomer (+)-propranolol were without effect on the pentagastrin response. In the rat isolated stomach preparation isoprenaline, salbutamol, salmefamol , adrenaline and nor-adrenaline all stimulated acid output over the range 2 X 10(-7) to 10(-5)M. These responses were antagonised by propranolol (2 X 10(-5)M), pindolol and timolol (10(-6)M) but only nor-adrenaline stimulated secretion was inhibited by the selective antagonists practolol, atenolol, butoxamine and ICI 118551. In vitro responses to beta-adrenoceptor agonists were not antagonised by atropine (10(-5)M), metiamide (10(-4)M) or prostaglandin E2 (10(-5)M).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Plasma digoxin concentrations in patients with atrial fibrillation and indications for the association with other antiarrhythmic agents.

The influence of practolol or verapamil on the activity of digoxin in atrial fibrillation has been studied in 16 hospitalized patients by determining plasma levels of the cardiac glycoside and its effects on the ventricular rate, before and during the association with each of the above drugs. Digoxin alone (0.25 mg/day p.o.) demonstrated a rather feeble activity, giving a satisfactory control of ventricular rate in only 3 patients. The association with low doses of practolol (50 or 100 mg twice a day p.o.) or with verapamil (80 mg three times a day p.o.) clearly improves the effects of digoxin. The action both of practolol and of verapamil is related to the pre-existing ventricular rate, the tachycardic patients being the most sensitive ones.

Aged↗