Ventricular fibrillation in type B Wolff-Parkinson-White syndrome.
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Adult↗
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The measurement of the relative efficacy of agonists by selective potentiation of tissue responses: studies with isoprenaline and prenalterol in cardiac tissue.
Isoprenaline, but not prenalterol, produced positive inotropy in guinea-pig papillary muscle. Prenalterol was a competitive antagonist of responses to isoprenaline in this tissue with a pKB of 7.24, as estimated by a Schild regression. Guinea-pig papillary muscles pretreated with the phosphodiesterase inhibitor, isobutylmethylxanthine (IMX), were 10 times more sensitive than controls to isoprenaline. In these tissues, prenalterol was a partial agonist producing 68% of the maximal response to isoprenaline. Schild regressions with atenolol indicated no change in beta-adrenoreceptors with IMX treatment and also that isoprenaline and prenalterol activated the same receptor in this tissue. The relative efficacy of isoprenaline and prenalterol was measured by using the KB estimated by Schild analysis for prenalterol and a Kd for isoprenaline from published binding studies. The relative efficacy of these drugs (epsilon ISO/epsilon PREN) was 242 +/- 29. The general method of potentiation of responses to weak agonists to estimate relative efficacy is discussed.
1-Methyl-3-isobutylxanthine↗
Comparison of the responses to drugs acting on adrenoreceptors and muscarinic receptors in human isolated corpus cavernosum and cavernous artery.
The contractile and relaxant effects of drugs which interact with adreno- and muscarinic receptors were investigated in isolated tissue from the human corpus cavernosum urethrae (CC) and the cavernous artery (Acc). Isolated CC preparations were contracted in a concentration-dependent fashion by noradrenaline (NA), phenylephrine and clonidine in the mentioned order of potency. Prazosin was 300 times more active than rauwolscine in inhibiting NA-induced contractions. In segments of the isolated Acc, clonidine was more potent than NA and phenylephrine, and prazosin and rauwolscine were about equieffective in inhibiting NA-induced contractions. Prazosin was more effective than rauwolscine in CC strips, and rauwolscine more effective than prazosin in Acc segments in inhibiting the noradrenergically mediated part of electrically induced contractions. Isoprenaline, prenalterol and procaterol each relaxed NA-contracted CC preparations in a concentration-dependent way; this effect was blocked by propranolol. Isoprenaline had no relaxant action in Acc segments. Neither acetylcholine (ACh) nor carbachol produced contraction in CC and Acc preparations. ACh, but particularly carbachol, had potent relaxant effects in NA-contracted CC preparations. This effect of ACh and carbachol was blocked by scopolamine. Relaxant, but less potent effects of the muscarinic receptor agonists were found in the Acc segments. It is suggested that there are important differences between penile arteries and erectile tissue proper in the response to adrenoreceptor and muscarinic receptor active drugs. The contractile effect of NA seems to be mediated mainly by alpha 1-adrenoreceptors in the CC and by alpha 2-adrenoreceptors in the Acc. It cannot be excluded that muscarinic receptor-mediated relaxation of NA-contracted CC preparations can be of importance for penile tumescence and erection.
Acetylcholine↗
Comparison of the cardiac effects of beta-adrenoreceptor agonists in anaesthetised and conscious dogs.
The cardiovascular effects of some beta-adrenoreceptor agonists on heart rate, blood pressure and myocardial contractility (maximum rate of change of left ventricular pressure/integrated isometric tension) were measured in pentobarbitone-anaesthetised and conscious, instrumented greyhounds. In anaesthetised dogs isoprenaline increased heart rate and myocardial contractility and reduced blood pressure. Prenalterol and RO 363, in equiactive inotropic doses, induced greater increases in heart rate than isoprenaline if blood pressure fell by less than 25 mmHg. Salbutamol had hypotensive activity at all doses and appeared to be a relatively selective inotrope. None of the agonists caused blood pressure to fall in the conscious dogs. Prenalterol and RO 363 were more effective inotropic stimulants, producing smaller increases in heart rate and more pronounced increases in myocardial contractility. Salbutamol, however, elicited greater increases in heart rate in the conscious animals and the inotropic selectivity demonstrated in the anaesthetised animals was lost. The direct effects of the beta-adrenoreceptor agonists, without modification by reflexes could be observed in the anaesthetised animals. The differences in the actions of the agonists in the conscious animals appear to be attributable to the state of the baroreceptor reflex control system and the relatively enhanced responsiveness of the heart.
Albuterol↗
Central and peripheral haemodynamic effects of prenalterol in patients with coronary heart disease.
The acute haemodynamic effects of prenalterol, a selective adrenergic beta-I-receptor agonist were studied in eight patients with coronary heart disease. Prenalterol was administered intravenously in four increasing doses to a cumulative dose of 5.6 mg. Fifteen minutes after the last dose of prenalterol two doses of the selective adrenergic beta-I-receptor antagonist metoprolol were administered intravenously to a cumulative dose of 17-5 mg. Ten minutes after each dose cardiac output, heart rate, arterial blood pressure, pulmonary artery pressure, systolic time intervals and forearm blood flow were determined. Haemodynamic effects of prenalterol: cardiac index and heart rate increased maximally by 38% and 39% respectively. Stroke index was increased by 6-9% after the first and second dose. Mean blood pressure was increased by 9.8 mmHg. Total peripheral resistance index was reduced by 19%. The mean pulmonary artery pressure decreased by 3.8 mmHg and pulmonary resistance index was reduced by 48%. Systolic time intervals were all reduced significantly after the second dose, which reflected the positive inotropic effects of prenalterol. Forearm blood flow increased by 29% and forearm vascular resistance was decreased by 20%. Haemodynamic effects of metoprolol: the haemodynamic changes induced by prenalterol were stepwise counteracted by metoprolol. After the second dose all the haemodynamic variables had returned to the control levels. It is concluded that prenalterol possesses a considerable positive inotropic as well as positive chronotropic effect on the myocardium. Both the chronotropic and inotropic effect of prenalterol was counteracted by metoprolol.
Blood Pressure↗
The actions of a new beta-adrenoceptor blocking drug, ICI 66082, on the rabbit papillary muscle and on the dog heart.
1 The actions of 4-(2-hydroxy-3-isopropylaminopropoxy) phenyl acetamide (ICI 66082), a new beta-adrenoceptor blocking drug, on the twitch response of the isolated papillary muscle of the rabbit and on dP/dt max and free heart rate of a denervated dog heart preparation, are described.2 ICI 66082 (up to 1 mg/ml) did not produce any depression of the twitch response of the rabbit papillary muscle. ICI 66082 antagonized the action of isoprenaline on this preparation at a concentration of 0.01 mug/ml.3 ICI 66082 (0.5-1.0 mg/kg intravenously) reduced the control value of dP/dt max in four dog preparations by a mean value of 529 mmHg/s (s.e. mean +/- 139 mm Hg/s), with no significant change in free heart rate. Antagonism of the effect of isoprenaline on dP/dt max and on free heart rate was demonstrated with ICI 66082 (0.1 mg/kg).4 ICI 66082 (1.0-1.5 mg/kg) produced no significant changes in dP/dt max or in free heart rate in four dogs pretreated with reserpine. A significant reduction (16% of the control value) in dP/dt max was observed with ICI 66082 at a high dose of 40-50 mg/kg.5 It is concluded that ICI 66082 is a competitive antagonist against the actions of isoprenaline on cardiac muscle, has no negative inotropic action (unless the dose exceeds 40 mg/kg) and lacks intrinsic sympathomimetic activity.
Acetamides↗
Central alpha- and beta-adrenoceptors modifying arterial blood pressure and heart rate in conscious cats.
1 In conscious unrestrained cats noradrenaline, alpha-methylnoradrenaline and clonidine, infused into the lateral cerebral ventricles (i.c.v.) caused dose-related falls in blood pressure and heart rate; both effects were abolished after i.c.v. phentolamine.2 In 12 out of 20 cats, i.c.v. isoprenaline and salbutamol when given caused dose-related pressor responses and tachycardias. These effects were abolished after i.c.v. beta-adrenoceptor blocking drugs but were unaffected by alpha-adrenoceptor blocking agents.3 In 5 out of 20 cats, i.c.v. isoprenaline regularly produced dose-related falls in blood pressure with associated tachycardias; both effects were abolished after i.c.v. beta-adrenoceptor blocking agents.4 Intracerebroventricular dopamine produced cardiovascular responses which were qualitatively similar to those produced by i.c.v. isoprenaline.5 Intracerebroventricular adrenaline produced complex responses in untreated animals but typical alpha-effects were obtained after prior i.c.v. treatment with a beta-adrenoceptor blocking agent and typical beta-effects after i.c.v. pretreatment with an alpha-adrenoceptor blocking agent.6 The cardiovascular changes produced by i.c.v. beta-adrenoceptor agonists were abolished after systemic administration of hexamethonium or bethanidine.7 The results are discussed in the light of the mode of action of beta-adrenoceptor stimulants and beta-adrenoceptor blocking agents in the treatment of hypertension.
Albuterol↗
Dissociation of beta-adrenoceptor-induced effects on amylase secretion and cyclic adenosine 3', 5' monophosphate accumulation.
By using a multi-channel microperifusion system the effects of noradrenaline, the beta1-adrenoceptor agonist prenalterol, and the beta2-selective agonist terbutaline were studied on amylase pig submandibular glands. 2 Noradrenaline caused significant amylase discharge and cyclic AMP accumulation. 3 Prenalterol was as effective as noradrenaline in causing amylase release but did not significantly affect the cyclic AMP content. 4 Terbutaline stimulated cyclic AMP accumulation, but had little effect on amylase secretion. 5 The present study reveals that there is a dissociation of the beta-adrenoceptor-induced amylase release and cyclic AMP formation, and that this dissociation may be due to different beta-adrenoceptor subtypes.
Amylases↗
Influence of heart rate on the effects of prenalterol on regional myocardial blood flow and function during coronary stenosis in dogs.
The effects of prenalterol, a selective beta 1-adrenoceptor agonist with potent cardiac positive inotropic properties have been investigated on regional myocardial blood flow (RMBF) (microspheres) and contractile function (ultrasonic crystals) during partial circumflex coronary artery stenosis in 8 open-chest anaesthetized dogs. Prenalterol was investigated at two intravenous doses: 5 micrograms kg-1, which increased myocardial contractility (dP/dt max: +29%) more than heart rate (+12%, up to 150 beats min-1) and 20 micrograms kg-1 which induced almost similar increases in contractility (+35%) and heart rate (+31% up to 175 beats min-1). The induced modifications of regional flow and function were then compared to those produced in another series of 6 dogs by atrial pacing at 150 and 175 beats min-1 respectively. Prenalterol significantly increased RMBF and segment length (SL)-shortening in a dose-dependent manner in the nonischaemic zone. In the ischaemic zone, RMBF was maintained and SL-shortening increased with prenalterol, 5 micrograms kg-1 whereas both RMBF and contractile function were severely decreased with prenalterol, 20 micrograms kg-1. Atrial pacing had almost no effect on RMBF and SL-shortening in the nonischaemic zone. In the ischaemic zone, atrial pacing rate-dependently decreased both RMBF and SL-shortening. Thus, a significant increase in contractility, associated with little tachycardia (prenalterol, 5 micrograms kg-1), induces beneficial effects on RMBF and function in both the nonischaemic and ischaemic myocardium. In contrast, a strong tachycardia, whether accompanied by positive inotropic effects (prenalterol, 20 gig kg-') or not (atrial pacing at 175 beats min-1) induces deleterious effects on RMBF and cardiac function in the ischaemic myocardium.
Adrenergic beta-Agonists↗
Clonidine in migraine prophylaxis.
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Adult↗
Potentiation by beta-adrenoceptor blocking agents of the inhibitory effect of adrenaline on carrageenin-induced rat paw oedema.
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Animals↗
A survey of the pharmacological properties of metoprolol in animals and man.
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Animals↗
Characterization of the adrenergic beta-receptor in the urinary bladder of man and cat.
The corpus-fundus of the urinary bladder of man and cat was studied in vitro with respect to type of beta-adrenergic receptors. In both species beta-adrenergic stimulation produced marked relaxation but species differences were apparent. In the cat bladder only beta1-receptors were found. In the human bladder the beta-receptors had neither beta1- nor beta2-characteristics. It is suggested that the beta-adrenergic receptors in the corpus-fundus of the human bladder are of a third type.
Acetylcholine↗
Effect of prenalterol, a beta-1-adrenoceptor agonist, on renin secretion rate in the anaesthetized dog.
The effects of the beta-1-adrenoceptor agonist, prenalterol, 20 microgram/kg intravenously on renin secretion rate (RSR), renal haemodynamics and sodium excretion were examined in anaesthetized dogs with innervated or denervated kidneys. In dogs with innervated kidneys, prenalterol increased RSR from 1.1 +/- 0.2 to 7.9 +/- 0.1 units X min.-1 X g-1 (P less than 0.01). Prenalterol did not affect mean arterial pressure, renal blood flow, glomerular filtration rate or sodium excretion. Heart rate was increased by 53 +/- 17 beats/min. (P less than 0.01). The increase in RSR produced by prenalterol was independent of intact renal innervation as RSR increased to the same extent in dogs with denervated kidneys. Pretreatment with the beta-1-adrenoceptor antagonist, metoprolol 0.5 mg/kg intravenously, abolished the increase in RSR produced by prenalterol. These findings suggest that prenalterol directly activates renal beta-1-adrenoceptors to increase RSR.
Adrenergic beta-Agonists↗
Actions of prenalterol, a new cardioselective beta1-agonist, terbutaline and isoprenaline on electrophysiological and mechanical parameters of guinea pig atrial and papillary muscles.
The electrophysiological and mechanical effects of prenalterol on the isolated guinea pig atrial trabeculae and papillary muscles were compared with those of terbutaline and isoprenaline. Isoprenaline was the most potent of the drugs tested on all parameters studied. Prenalterol, on the other hand, failed to induce any changes in the atrial action potentials. The action potential duration was shortened in the atrial trabeculae by terbutaline and isoprenaline. All three substances shortened the action potential in the papillary muscles. In addition, isoprenaline increased the plateau height, and like terbutaline, increased the rate of repolarization during phase 3. Neither prenalterol nor terbutaline changed the effective refractory period in the atrial trabeculae whereas isoprenaline shortened it. All three substances shortened this parameter in the papillary muscles. The developed force and the rate of developed force were increased by all three substances. In addition, the total twitch duration was decreased.
Action Potentials↗
Characterization of mechanical effects and beta-adrenoceptor binding of prenalterol in rat myocardium.
The partial beta-agonist prenalterol has been found to differ from the full agonist isoprenaline in some aspects of its cardiac action. We therefore studied in rat myocardium whether prenalterol elicited the same qualitative changes of the contraction-relaxation cycle as was previously found for isoprenaline. We also measured binding of prenalterol to beta-adrenoceptors. Prenalterol augmented relaxation more than contraction and thus evoked the same qualitative changes of the contraction-relaxation cycle as did isoprenaline. However, the response developed slower than that to isoprenaline, and the effect on relaxation followed a more protracted time course than the effect on contraction. Prenalterol bound non-selectively to beta 1- and beta 2-adrenoceptors in both heart and lung broken cell preparations. pKd for binding to beta-adrenoceptors and pD2 values for functional effects in heart were similar, i.e. prenalterol had to occupy half the amount of beta-adrenoceptors in order to evoke half-maximal functional effects. The non-selective alpha-blocker phentolamine potentiated the effects of prenalterol on contraction, but did not change the equilibrium binding of prenalterol to cardiac beta-adrenoceptors. Phentolamine did not change the potency and efficacy of isoprenaline. Thus, although prenalterol qualitatively evoked the same response as isoprenaline, it also exhibited some properties which differed.
Animals↗
Lack of functional influence by prenalterol through alpha 1-adrenoceptors in rat myocardium.
Some of the cardiac properties of the partial beta-agonist prenalterol may indicate a contribution from alpha 1-adrenergic stimulation. We therefore studied whether prenalterol interacted with alpha 1-adrenoceptors in rat myocardium. Combination with propranolol did not reveal an alpha 1-adrenergic inotropic effect of prenalterol in papillary muscles. Neither did prenalterol block the alpha 1-adrenergic response to phenylephrine. In myocardial cells, prenalterol inhibited 3H-prazosin binding to alpha 1-adrenoceptors only at very high concentrations. Prenalterol thus exhibited no functionally important interactions with alpha 1-adrenoceptors in myocardium, and its properties cannot be accounted for in terms of contribution from alpha 1-adrenergic effects.
Animals↗
Arrhythmogenic assessment of prenalterol in conscious dogs.
Possible arrhythmogenic side-effects of the positive inotropic agent prenalterol were studied in conscious dogs, three to four days after coronary artery ligation. Prenalterol showed a propensity to cause arrhythmias in one out of eight dogs, thereby confirming published data from clinical studies.
Animals↗