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PubMedDate not supplied

Interaction in healthy volunteers between prenalterol, a selective beta 1-adrenoceptor agonist, and metoprolol or propranolol.

We studied the hemodynamic effects of the selective beta 1-adrenoceptor agonist prenalterol in healthy subjects before and after intravenous infusion of the nonselective beta-adrenoceptor blocker propranolol or the beta 1-selective adrenoceptor blocker metoprolol. Intravenous infusions of 0.1, 0.25, and 0.5 mg prenalterol induced a dose-dependent decrease in total electromechanical systole and pre-injection period, whereas left ventricular ejection time remained unchanged. Stoke volume as determined by impedance cardiography was not changed, but a dose-dependent increase in cardiac output due to an increase in heart rate was observed. Systolic blood pressure was significantly increased, but diastolic blood pressure remained unchanged. After intravenous administration of either 10 mg propranolol or 20 mg metoprolol, prenalterol was infused in a 10 times higher dose than before. The hemodynamic effects were similar to those observed before the beta-blockers. Whether propranolol or metoprolol was administered did not influence the effects induced by prenalterol. It is suggested that prenalterol might be a useful drug to counteract undesired hemodynamic effects of beta-adrenoceptor blockers.

Adrenergic beta-Agonists↗

PubMedDate not supplied

Comparative effects of prenalterol and dobutamine in a canine model of acute ischemic heart failure.

The hemodynamic effects of the inotropic agents prenalterol and dobutamine were compared in a canine model of acute ischemic heart failure following two-vessel coronary artery constriction. Intravenous infusions of both inotropic agents resulted in improvement of cardiac output, left ventricular maximum dP/dt, and contractile force in the nonischemic zone and in a decrease in systemic vascular resistance. No significant changes occurred in ischemic zone contractile force or left ventricular end-diastolic pressure following either inotropic agent compared to saline controls. Significant differences between the two inotropic agents consisted of prenalterol's markedly longer duration of action (hemodynamic half life of 3 hr after discontinuation compared to a value of 1.7 min after dobutamine discontinuation) and greater augmentation of cardiac output at high-dose dobutamine due to greater increases in heart rate. However, similar hemodynamic effects were noted with prenalterol and dobutamine at doses which increased nonischemic contractile force 50%. Both inotropic agents were associated with ventricular arrhythmias in the acute ischemic state. Implications regarding the use of prenalterol and dobutamine in clinical acute ischemic low-output states are discussed.

Animals↗

PubMedDate not supplied

Effects of in vivo beta-adrenoceptor down-regulation on cardiac responses to prenalterol and pirbuterol.

The effects of beta-adrenoceptor down-regulation on rat left atrial responses to the full agonist isoproterenol and the partial agonists prenalterol and pirbuterol were studied. Atria from rats implanted with a mini-osmotic-pump subcutaneously delivering isoproterenol at 400 micrograms X kg-1 X h-1 for 4 days were 12-16 times less sensitive to isoproterenol than normal atria. Scatchard analyses indicated that the implantation of these mini-osmotic-pumps produced a 50% decrease in the number of beta-adrenoceptors in the ventricles with no alteration in the binding constant of [3H]dihydroalprenolol. Receptor down-regulation produced a parallel shift to the right of concentration-response curves to isoproterenol, and a complete suppression of responses to both partial agonists. The affinities of the partial agonists for the receptors were not altered; in desensitized atria the partial agonists were functional beta-antagonists blocking the responses to isoproterenol. The data are modeled by equations from classical receptor theory which predict the depression of responses to partial agonists with receptor down-regulation. These results are discussed with respect to the utility of prenalterol and pirbuterol in congestive heart failure since possible tachyphylaxis to these drugs with chronic usage could limit their value.

Adrenergic beta-Agonists↗

PubMedDate not supplied

Selectivity of prenalterol for adrenergic receptor subtypes: a potential mechanism of inotropic selectivity.

To address the hypothesis that myocardial adrenergic receptors mediating chronotropy may be distinguishable from receptors mediating inotropy on the basis of existing subtype classifications, the binding properties of the inotropically selective adrenergic agonist prenalterol to receptor populations of known subtype were characterized. In competitive binding assays, prenalterol exhibited higher affinity for beta 1- than for beta 2-receptors, and a low affinity for both alpha 1- and alpha 2-receptors, in comparison with non-subtype-selective agonists. In addition, log molar displacement curves for prenalterol binding to beta 1-receptors, but not to beta 2- or alpha 2-receptors, were steepened and shifted rightward by guanine nucleotide, suggesting that prenalterol is a beta 1-agonist, but may have antagonist properties at beta 2- and alpha 2-receptors. This receptor subtype profile is similar to that of dobutamine, another inotropically selective adrenergic agonist. This concordance lends further support to the hypothesis that chronotropic responses to exogenous adrenergic agonists may be mediated selectively through beta 2-receptors.

Adrenergic beta-Agonists↗

PubMedDate not supplied

Contractile, coronary, and metabolic effects of the acute and long-term treatment of cardiac failure with prenalterol.

Prenalterol was examined with regard to its acute intravenous effects on left ventricular function, coronary hemodynamics, and myocardial oxygen consumption, as well as for its long-term effects, by oral therapy, on left ventricular function and systemic hemodynamics. Intravenous prenalterol enhances myocardial contractility and left ventricular ejection function significantly. A decrease in total peripheral vascular resistance is effected. Myocardial oxygen consumption is only moderately increased, most probably because of the decrease in the systolic integrated wall stress of the left ventricle. The changes of coronary circulation (blood flow, resistance, arteriovenous, oxygen difference) indicate benign and metabolically induced coronary vasodilation. Long-term oral treatment of patients with severe cardiac failure by prenalterol effects significant enhancement in-left ventricular performance within the first 1-2 months of treatment; however, this effect is not present at longer therapy intervals (16-28 weeks). Tolerance development as well as the natural history of these patients may be responsible for this inotropic amelioration. There were no clinical side effects with either intravenous or oral application. It may be concluded that prenalterol is highly effective in acute cardiac failure (intravenous administration) and also in chronic heart disease (long-term oral application). However, the long-term effects are unpredictable, and tolerance development has to be considered.

Administration, Oral↗

PubMedDate not supplied

Effects of a beta 1-adrenoceptor agonist, prenalterol, on renal function and renin secretion rate in anesthetized dogs.

Experiments were conducted to examine the effects of prenalterol on renal function and renin secretion in anesthetized dogs. Specifically, we tested whether prenalterol alters renal function directly, or only indirectly as a consequence of a systemic action of the drug. Accordingly, prenalterol was infused into one renal artery for five consecutive 15-min periods, at incremental rates of 0.1, 0.3, 0.9, 2.7, and 8.1 micrograms X kg-1 X min-1. Heart rate and mean arterial blood pressure were recorded, and renal functions and renin secretion rates were measured bilaterally. Direct intrarenal prenalterol infusion caused a 60 bpm increase in heart rate and resulted in marked increases in renin secretion rates from both kidneys. Intrarenal prenalterol infusion also reduced urinary sodium and potassium excretions bilaterally and equally. There were no consistent changes in mean arterial blood pressure, or in glomerular filtration rate or renal blood flow, during prenalterol infusion. We conclude that although prenalterol increases renin secretion rate markedly and may alter renal electrolyte excretion, these effects are not mediated by a direct intrarenal action of the drug.

Adrenergic beta-Agonists↗

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↗

PubMedDate not supplied

Role of cyclic AMP in cardiac beta-adrenoceptor desensitization: studies using prenalterol and inhibitors of phosphodiesterase.

We examined the effects of prolonged exposure of cardiac cells in primary culture to the partial beta-adrenoceptor agonist prenalterol and inhibitors of phosphodiesterase on their subsequent ability to increase intracellular cyclic AMP during a 5-min exposure to 50 microM isoprenaline (receptor responsiveness). Although prenalterol possesses only 7% of the agonist activity of isoprenaline on adenylate cyclase, it induces extensive beta-adrenoceptor desensitization. Three hours after exposing the cells to 1 microM prenalterol, beta-adrenoceptor responsiveness was reduced by 40% (p less than 0.05), whereas after 12 h the reduction averaged 55%. Prolonging the incubation time to 48 h had no further effect on the magnitude of receptor desensitization. The magnitude of the desensitization was concentration dependent. On exposure of cells to 10(-8) M prenalterol for 16 h, receptor responsiveness was reduced by 19%, and at concentrations of 1 microM and higher responsiveness was reduced by 60% (p less than 0.01). Receptor desensitization appeared to be due to an inability of receptors to activate adenylate cyclase as well as to receptor loss. To investigate if beta-adrenoceptor desensitization as well as receptor loss could be mediated by cyclic AMP, the cells were exposed for 16 h to inhibitors of phosphodiesterase. Exposure of cells to the phosphodiesterase inhibitor isobutylmethylxanthine (0.1 mM) (which increased intracellular cyclic AMP by between 50 and 150%) also induced receptor desensitization. The reduction in receptor responsiveness averaged 62% (p less than 0.01). The loss in responsiveness could be accounted for by an inability of receptors to activate adenylate cyclase as well as by receptor loss.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗

PubMedDate not supplied

Effect of prenalterol on contractility, relaxation, and filling phase in coronary artery disease patients with previous myocardial infarction.

Twelve postmyocardial infarction patients, with angiographically proven asynergic areas, but without overt cardiac failure, were treated with prenalterol intravenously, (a new cardioselective inotropic agent) at a dose of 30 micrograms/kg. The aim of this study was to test the usefulness and safety of this new drug in postmyocardial infarction patients, monitoring systolic and diastolic acute hemodynamic changes. Significant improvement in cardiac contractility was demonstrated by the increase of ejection fraction (+23%), stroke volume index (+22%), cardiac output (+41%), positive dp/dt (+82%), and Vmaxd (+39%). Left ventricular systolic, mean aortic, and mean right atrial pressure remained unchanged; a slight decrease in end-diastolic volume index (-2%) occurred. A significant increase in heart rate (from 66 +/- 7 to 85 +/- 14 beats/min), without electrocardiographic changes or subjective complaints of angina pectoris, was observed. Segmental wall motion analysis showed an improved systolic shortening in normal (from 34 to 44%) and in asynergic areas (from 10 to 18%), whereas no changes were observed in dyskinetic areas. The relaxation and filling phase also improved, as tested by negative dp/dt (+39%), time constant of relaxation (-36%), and by indices of ventricular compliance. Side effects consisted of a slight feeling of tension in two patients and a short episode of ventricular tachycardia (5 beats) in another patients. No episode of angina pectoris was observed. These results, with special emphasis on lack of exacerbation of pre-existing ischemia (although obtained in patients without evident heart failure), suggest the potential usefulness of prenalterol in acute cardiac failure, as well as postmyocardial infarction low-output syndrome.

Adrenergic beta-Agonists↗

PubMedDate not supplied

Hemodynamic and myocardial metabolic effects of the beta-agonist prenalterol in ischemic left ventricular dysfunction.

Hemodynamic and myocardial metabolic parameters in ischemic left ventricular (LV) dysfunction were evaluated in response to the beta-agonist prenalterol. Twenty micrograms/kg intravenous prenalterol increased resting heart rate and cardiac output and decreased LV filling pressure, systemic vascular resistance, and pulmonary artery pressure. Resting coronary blood flow and myocardial oxygen consumption increased but net myocardial lactate and oxygen extraction did not change significantly. During pacing induced tachycardia (121 +/- 4 beats/min), prenalterol improved cardiac index and stroke work index; whereas, LV filling pressure, systemic vascular resistance, and pulmonary artery pressure decreased. Coronary blood flow and myocardial oxygen extraction did not change significantly. Net myocardial lactate extraction during pacing decreased insignificantly; one patient developed overt lactate production. Thus, prenalterol improves cardiovascular function at rest and during pacing-induced tachycardia in ischemic LV failure, but at the cost of higher resting myocardial oxygen consumption. The majority of subjects had no adverse metabolic response.

Adrenergic beta-Agonists↗

PubMed1976