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PubMed1984

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↗
PubMed1983

Hemodynamic, hormonal and electrolyte responses to prenalterol infusion in heart failure.

The hemodynamic, hormonal and electrolyte effects of prenalterol, a synthetic selective beta 1 agonist, were studied in six patients with New York Heart Association functional class II and III heart failure. Prenalterol was infused incrementally at 60, 120 and 240 nmol/min, each rate for 24 hours, producing steady-state plasma prenalterol levels of 52 +/- 3, 121 +/- 6 and 194 +/- 9 nmol/1, respectively (mean +/- SEM). Hemodynamic and hormonal measurements were performed before, during and after prenalterol administration under conditions of constant body posture and a regulated intake of dietary sodium and potassium. Prenalterol induced a statistically significant increase in cardiac index (from 2.6 +/- 0.2 to 3.1 +/- 0.3 1/min/m2), with parallel increases in stroke index (from 28 +/- 2 to 34 +/- 2 ml/beat/m2). Forearm blood flow measurements increased (from 2.9 +/- 0.5 to 4.1 +/- 0.6 ml/min/100 g), while calculated systemic vascular resistance fell, as did pulmonary capillary wedge pressure (from 13.7 +/- 1.6 to 10.5 +/- 1.7 mm Hg). The drug did not alter heart rate, arterial pressure, right heart pressures or the frequency of ventricular premature beats. Prenalterol increased plasma renin activity (from 2.9 +/- 0.8 to 6.6 +/- 1.8 nmol/1/hour), angiotensin II (from 59 +/- 12 to 89 +/- 22 pmol/1), urinary aldosterone excretion (from 41 +/- 10 to 78 +/- 34 nmol/day) and plasma insulin (from 10.6 +/- 2.2 to 19.8 +/- 3.9 mU/1). Circulating catecholamines, cortisol, glucose, glucagon or pancreatic polypeptide did not change. Dose-response studies in five patients showed dose-dependent increments in hemodynamic variables, while hormonal changes plateaued at the second dose level. We conclude that prenalterol infusion augments myocardial contractility, reduces systemic vascular resistance, and stimulates insulin release and the renin-angiotensin-aldosterone system.

Dose-Response Relationship, Drug↗
PubMed1984

Effects of in vivo treatment with isoprenaline or prenalterol on beta-adrenoceptor mechanisms in the heart and soleus muscle of the cat.

The full agonist isoprenaline (5.3-6.6 nmol/kg . min) and the partial beta-adrenoceptor agonist prenalterol (10.6-13.3 nmol/kg . min) were administered to cats continuously via osmotic minipumps (i.p.). After seven days the functional and adenylate cyclase responsiveness to the agonists, as well as the beta-adrenoceptor-binding characteristics, were studied in cardiac and soleus muscle preparations in vitro. After isoprenaline pretreatment, the papillary muscles and soleus muscle strips wer 15-18 times less sensitive to isoprenaline compared with muscles from control cats. The stimulatory potency (pD2) of prenalterol in the papillary muscle was not changed significantly. The affinity of the agonists to the beta-adrenoceptors was unaffected in both tissues by the pretreatment, but the densities of beta-adrenoceptors were significantly reduced, by 36% (myocardium) and 47% (soleus) respectively. In the cat papillary muscle the intrinsic sympathomimetic activity (ISA) of prenalterol on contractile parameters was reduced from 84 (Tmax), 69 (dT/dtmax) and 71% (dT/ dtmin ) in control animals, to 33, 22 and 28%, respectively in the animals pretreated with isoprenaline. Prenalterol pretreatment did not induce any marked changes, either in the stimulatory potency or affinity of the agonists in the two tissues or in the maximal response (ISA) of prenalterol in the papillary muscle. The marked reduction in the stimulatory potency of isoprenaline and the reduced ISA of prenalterol in the myocardium after isoprenaline pretreatment can not be explained by the reduction in beta- adrenoceptor density alone. Since the affinity to the beta- adrenoceptors is unaffected, a reduced efficiency in the signal transmission must be the main cause.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1982

Cardiostimulatory effects of prenalterol, a beta-1 adrenoceptor partial agonist, in vivo and in vitro. Correlation between physiological effects and adenylate cyclase activity.

The cardiostimulatory effects of prenalterol, a beta-1-adrenoceptor partial agonist, were studied in vivo and in vitro and compared to those evoked by isoprenaline, a full agonist, and to those of other partial agonists. In the anaesthetized rat, prenalterol and terbutaline were found not to elevate the myocardial cyclic AMP content; this was in sharp contrast to isoprenaline. Both partial agonists did, however, produce significant effects on heart rate. In the anaesthetized cat, prenalterol exhibited chronotropic and inotropic intrinsic activities of 88 and 76% respectively in relation to isoprenaline. No statistically significant increase in myocardial cyclic AMP content could however be detected. Prenalterol did not stimulate adenylate cyclase significantly in the cat myocardial homogenate. This was also true of the beta-2-adrenoceptor selective partial agonist procaterol. In this preparation, isoprenaline, noradrenaline and adrenaline acted as full agonists. Furthermore, prenalterol produced a concentration-dependent inhibition of isoprenaline-activated adenylate cyclase. Our data indicate that maximal cardiac stimulation occurs at a low level of adenylate cyclase activation and low myocardial cyclic AMP concentration when provoked by a full beta-adrenoceptor agonist. The maximal physiological effects of a partial agonist such as prenalterol may consequently be achieved at a marginal activation of the adenylate cyclase. The present data may thus support the hypothesis of a large beta-adrenoceptor reserve for full agonists in the heart.

Adenylyl Cyclases↗
PubMed1980

Metabolic and haemodynamic effects and pharmacokinetics of a new selective beta 1-adrenoceptor agonist, prenalterol, in man.

The metabolic and haemodynamic effects of three intravenous doses (0.5, 1.0 and 4.0 mg) of prenalterol, a selective beta 1-adrenoceptor agonist, were studied in 10 healthy male subjects. Plasma levels of prenalterol during the experiments were related to the haemodynamic effects. Prenalterol induced a dose-dependent increase in systolic blood pressure and heart rate. The maximal effects amounted to about 30 mm Hg and 15 beats/min, respectively, after the highest dose (4.0 mg). The diastolic blood pressure fell by a maximum of about 15 mm Hg. The effect of prenalterol on systolic blood pressure and heart rate persisted for about 3 h after the end of the last infusion, whereas that on diastolic blood pressure only lasted for 60 min. Compared with placebo, there was a moderate increase in plasma FFA and glycerol. A small rise in insulin level was also recorded, but no significant change was seen in other metabolic variables--triglycerides, glucose, lactate pyruvate. Serum potassium tended to decrease and serum sodium was unchanged. The initial distribution of prenalterol was rapid (half-life 7 min) and the overall elimination rate corresponded to a plasma half-life of 2 h. A linear relationship was found between the plasma level of prenalterol and its effects on systolic blood pressure and heart rate.

Adrenergic beta-Agonists↗
PubMed1980

Immediate haemodynamic effects of prenalterol, a new adrenergic beta-1-receptor agonist, in healthy volunteers.

The acute haemodynamic effects of prenalterol, a selective adrenergic beta-1-receptor agonist, were studied in eight healthy male volunteers. Prenalterol was administered i.v. in five increasing doses to a cumulative dose of 5.55 mg. After the last dose of prenalterol, three doses of the selective adrenergic beta-1-receptor antagonist metoprolol were administered i.v. to a cumulative dose of 17.5 mg. After each dose, cardiac output (CO), stroke volume (SV), blood pressure (BP), heart rate (HR), systolic time intervals (STI) and forearm blood flow (FBF) were determined. Prenalterol had the following effects: CO was significantly increased by 21.0% after the fourth dose, but the fifth dose did not further change CO. SV was unchanged after the first four doses, but after the fifth dose a significant decrease in SV of 7.0% was seen. Mean BP was increased significantly by 7.7%, but diastolic BP remained unchanged. HR was increased by 28.4%. Total peripheral resistance was reduced by 8.8%. STI were reduced significantly after the second dose, which indicates that prenalterol has a positive inotropic action. FBF was increased significantly after the fourth dose. After the third dose of metoprolol, the CO, SV, means BP, HR, STI and FBF had returned to their control values. It is concluded that prenalterol has positive inotropic and chronotropic effects on the myocardium, and that metoprolol is a specific antidote.

Adolescent↗
PubMed1983

Ventilatory and haemodynamic effects of prenalterol and terbutaline in asthmatic patients.

In 8 asthmatic patients a comparative study was performed of the ventilatory and haemodynamic effects of the beta 1-receptor stimulator prenalterol and the beta 2-receptor stimulator terbutaline infused in increasing doses after a placebo. Terbutaline caused a dose-dependent decrease in diastolic blood-pressure (BP) and an increase in systolic BP and heart-rate (HR), while mean arterial pressure (MAP) did not change. Prenalterol produced a dose-dependent increase in MAP and systolic BP, while diastolic BP was unaffected. HR was increased only by the largest dose of prenalterol. The haemodynamic effects of the terbutaline infusion can be explained by a reflex response to the vasodilatation induced by stimulation of the vascular beta 2-receptors, while the effects of prenalterol can mainly be accounted for by a direct action on beta 1-receptors in the heart. These observations show that the cardiac side-effects of beta 2-agonists cannot be avoided by producing more selective agonists. Terbutaline caused a dose-dependent increase in the ventilatory indices. Prenalterol in larger doses caused a limited but significant increase in the ventilatory indices, comparable to the decrease in ventilation caused by the beta 1-selective blocker metoprolol. These findings suggest that the ventilatory effects of metoprolol and prenalterol are mediated via beta 1-receptors in the airways, which apparently play a functional role in asthma.

Adrenergic beta-Agonists↗
PubMed1984

Intravenous and oral prenalterol in congestive heart failure. Effects on systemic and coronary hemodynamics and myocardial catecholamine balance.

Systemic and coronary hemodynamic effects of prenalterol, a beta-1 receptor agonist, were determined in patients with chronic congestive heart failure, initially after intravenous administration (10 patients) and then after oral administration (eight patients). Cardiac index increased by 33 percent and 30 percent after intravenous and oral prenalterol, respectively. The increase in stroke volume index and stroke work index and decrease in pulmonary capillary wedge pressure and systemic vascular resistance were not significant. Myocardial oxygen consumption and coronary sinus blood flow increased in the majority of patients, although these changes were not statistically significant. There were no significant changes in transmyocardial norepinephrine or epinephrine balance. The systemic and coronary hemodynamic effects of both intravenous and oral prenalterol were similar. Major side effects included sudden death (two patients) and hypotension and bradycardia (three patients) during oral prenalterol treatment. It is concluded that improved left ventricular function following both intravenous and oral prenalterol may be associated with increased myocardial oxygen consumption, and serious adverse effects may occur during prenalterol therapy.

Administration, Oral↗
PubMed1983

Electrophysiologic properties of prenalterol.

We assessed the electrophysiological properties of prenalterol, a new beta-selective agonist, in 10 patients with normal and 10 patients with delayed atrioventricular (A-V) conduction times. We evaluated sinus node function, A-V conduction times, refractory periods, atrial or ventricular arrhythmias, spontaneous or induced by the single extrastimulus technique during basal conditions, 5 minutes after a first dose of 20 micrograms/kg of prenalterol, and 5, 15 and 30 minutes after a second injection of the same dose. Prenalterol increased heart rate about 20%, with statistically significant shortening of right atrial refractory periods, A-V nodal functional and effective refractory periods and A-H interval in both groups after the first dose. In the 6 patients with sick sinus syndrome, prenalterol increased heart rate significantly and decreased maximum sinus node recovery time which reached a statistically significant value (P less than 0.05) 5 and 30 minutes after the second dose. At the highest dose, prenalterol seemed to increase the number of ventricular and/or atrial arrhythmias only in those patients with the arrhythmias before treatment. Prenalterol increases heart rate and decreases A-V node conduction times. The shortening of maximum sinus node recovery time in patients with the sick sinus syndrome, especially if confirmed after oral administration, could indicate a specific use of this drug in patients with sinus bradycardia or atrial fibrillation with a slow ventricular response.

Adrenergic beta-Agonists↗
PubMed1988

Increase of cyclic AMP in subcellular fractions of rat heart muscle after beta-adrenergic stimulation: prenalterol and isoprenaline caused different distribution of bound cyclic AMP.

Although prenalterol is a partial beta-agonist, it has been reported to produce only a marginal, non-significant increase of cAMP in rat hearts. We studied the effect of prenalterol and isoprenaline on free and bound cAMP content in subcellular fractions of perfused rat hearts to see whether prenalterol increased cAMP and whether there were differences in the subcellular distribution of the cAMP contents after stimulation with the drugs. The in situ binding characteristics of cAMP to the protein kinases at different degree of beta-adrenergic stimulation were elucidated. Prenalterol increased significantly both total cAMP content in homogenate, bound cAMP in a 100,000 g particulate fraction and bound, free and total cAMP contents in the resulting supernatant. While prenalterol increased bound cAMP in the particulate fraction and in the supernatant proportionally, isoprenaline caused a relatively greater increase of bound cAMP in the supernatant. At equieffective concentrations regarding inotropic and lusitropic effects, prenalterol and isoprenaline increased bound cAMP in the particulate fraction to the same degree, while the increase in the other fractions was greater after isoprenaline. Thus, the cAMP bound in the particulate fraction seemed to determine the inotropic state of the cell after beta-adrenergic stimulation, supporting a compartmentation of cAMP in myocardium. In controls 31 to 34% of the total binding capacity for cAMP in the particulate fraction was occupied, increasing to 77% after maximal beta-stimulation. The binding capacity in the supernatant was only 15 to 18% saturated in the basal situation and about half saturated after maximal beta-stimulation. cAMP bound in the particulate fraction is of special interest when cAMP and functional effects are studied.

Animals↗
PubMedDate not supplied

A comparison of the hemodynamic effects of prenalterol and isoprenaline in patients with complete heart block.

Prenalterol is a new beta-adrenergic agonist which stimulates mainly beta 1-receptors, in contrast to isoprenaline which stimulates both beta 1- and beta 2-receptors. We studied the hemodynamic effects of prenalterol and isoprenaline in seven patients with complete heart block and idioventricular escape rhythm due to ischemic heart disease. Isoprenaline was given as a continuous infusion at two increasing doses (1.7 micrograms/min and 3.4 micrograms/min each given for 30 min). After the second dose of isoprenaline the cardiac index was increased from 2.27 +/- 0.06 to 3.61 +/- 0.60 1/min/m2, heart rate was increased from 34.1 +/- 1.2 to 50.4 +/- 3.1 beats/min and mean blood pressure was decreased by 12.4 mm Hg. Mean pulmonary artery pressure was increased by 2 mm Hg. Prenalterol was given as two i.v. bolus injections of 3.5 mg and 7.0 mg at 15-min intervals. The first dose of prenalterol increased the cardiac index from 2.22 +/- 0.10 to 2.42 +/- 0.12 and heart rate from 37.0 +/- 1.8 to 40.1 +/- 1.7. Mean blood pressure and mean pulmonary artery pressure were unchanged. The second dose of prenalterol did not change the hemodynamic variables significantly compared to the changes after the first dose. We conclude that isoprenaline is preferable to prenalterol for treatment of complete heart block.

Adrenergic beta-Agonists↗
PubMed1988

The selectivity of xamoterol, prenalterol, and salbutamol as assessed by their effects in the presence and absence of ICI 118,551.

The selectivity of single oral doses of xamoterol, 200 mg, prenalterol, 50 mg, and salbutamol, 8 mg, was compared in eight healthy male volunteers by measuring their effects on sleeping heart rate, supine heart rate, blood pressure, forearm blood flow, finger tremor, and exercise heart rate in the presence and absence of the specific beta 2-adrenoceptor antagonist ICI 118,551, 25 mg. Xamoterol, 200 mg, increased sleeping heart rate and systolic blood pressure, decreased exercise heart rate, and had no effect on diastolic blood pressure, forearm blood flow, or finger tremor. The concurrent administration of ICI 118,551, 25 mg, did not alter these results. Supine heart rate was increased by xamoterol and did not differ from that for xamoterol with ICI 118,551. Prenalterol, 50 mg, increased sleeping heart rate, supine heart rate, systolic blood pressure, forearm blood flow, and finger tremor, decreased diastolic blood pressure, and had no effect on exercise tachycardia. The concurrent administration of ICI 118,551 with prenalterol reduced the increase in sleeping heart rate, supine heart rate, and forearm blood flow, and reduced the fall in diastolic blood pressure caused by prenalterol alone. The increase in finger tremor following prenalterol with ICI 118,551 tended to be less than that following prenalterol. Salbutamol, 8 mg, increased sleeping heart rate, supine heart rate, systolic blood pressure, forearm blood flow, finger tremor, and exercise heart rate, and caused a fall in diastolic blood pressure. When salbutamol, 8 mg, was administered with ICI 118,551, 25 mg, the only changes detected were a small initial increase in finger tremor and a small rise in diastolic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1982

Metabolic effects of prenalterol in healthy volunteers.

The effect of the beta 1-adrenoceptor agonist prenalterol on the metabolic parameters glucose, lactate, free fatty acids and serum-insulin were studied in 8 healthy volunteers. Prenalterol was administered intravenously in geometrically increasing doses from 5 to 80 micrograms/kg. The only metabolic effect of prenalterol that could be proved was a significant dose-dependent rise in FFA-concentration. The stimulating effect of prenalterol on lipolysis was significant not only at the time points of maximal effect following each injection, but also 30 min later. Serum-insulin-concentration and glucose- and lactate-concentration failed, however, to show a significant rise after prenalterol administration. This behaviour is a strong indication of a beta 1-selectivity of prenalterol over the whole dose range given.

Adrenergic beta-Agonists↗
PubMed1981

The effects of intravenous prenalterol on ventricular performance, as assessed by radionuclide ventriculography, in patients with ischaemic heart disease.

1 We have observed the effects of intravenous prenalterol (1 mg and 2 mg) on ventricular performance, assessed by radionuclide ventriculography, in nine patients with ischaemic heart disease with varying degrees of impairment of ventricular performance. In seven of these patients the effects of prenalterol were compared with those of isoprenaline infused at 1 microgram/min. 2 Prenalterol caused no significant increase in heart rate, but systolic blood pressure increased by 26% (P less than 0.002). In contrast, isoprenaline caused heart rate to increase by 22% (P less than 0.02) and diastolic blood pressure to fall by 9% (P less than 0.01). 3 Left ventricular ejection fraction (LVEF) increased with both drugs, but the increase was greater with isoprenaline, as was the fall in the ratio mean ejection time: left ventricular ejection time, which is an index of improved ventricular performance. 4 Because of the increased heart rate and stroke volume produced by isoprenaline, cardiac output increased 45% above control values (P less than 0.001), but the increase in cardiac output after prenalterol did not reach statistical significance. 5 In three patients with very poor ventricular function (LVEF less than 0.30) prenalterol had little effect on ejection fraction, and caused increased regional ventricular dyskinesia. 6 The increase in systolic blood pressure, and therefore cardiac afterload brought about by prenalterol may limit ventricular response. The response might be enhanced by the addition of vasodilator therapy.

Blood Pressure↗
PubMedDate not supplied

Haemodynamic effects of prenalterol in acute myocardial ischaemia in open chest pigs.

The haemodynamic effects of prenalterol, a new sympathomimetic agent, have been studied in anaesthetized open-chest pigs with acute myocardial ischaemia provoked by left anterior descending coronary artery ligation. A group of eight animals was infused with saline and served as control (C). In both groups the ligation of the left anterior descending coronary artery determined a significant (P less than 0.05) reduction of aortic flow, maximum left ventricular (LV) dp/dt with no changes in heart rate. The infusion of a first dose of 30 micrograms/kg of prenalterol restored the depressed haemodynamics but increased significantly the heart rate in the prenalterol group while the saline infused group did not show any significant changes. The haemodynamic effects of prenalterol were still evident 25 min after the infusion. The subsequent administration of a second dose of 60 micrograms/kg of prenalterol resulted in a further improvement of the aortic flow, LV dp/dt and heart rate which reached values higher than in the basal condition. The positive inotropic effect was not associated with changes in stroke volume, therefore the increase in aortic flow was essentially due to an increase of the heart rate. It is concluded that prenalterol is a powerful inotropic agent in acutely infarcted animals. Its action on aortic flow appears to be related to an increase in heart rate in contrast to some previous observations.

Animals↗
PubMed1984

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↗
PubMed1981

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↗
PubMed1983

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↗