ABSTRACT
The mechanism of the positive inotropic effect of prostacyclin (PGI2) (2.6 x 10(-6) mol/l) on the isolated right ventricle of rat heart was studied. Our results show that the positive inotropic effect of prostacyclin is produced indirectly through beta adrenoceptors and slow Ca2+ channels, because blockade of slow Ca2+ channels with verapamil (10(-6) mol/l) and beta adrenoceptors with propranolol (10(-6) mol/l) abolishes this effect. Alpha adrenoceptors do not mediate the action of PGI2.
Subject(s)
Epoprostenol/pharmacology , Myocardial Contraction/drug effects , Adrenergic alpha-Antagonists/pharmacology , Adrenergic beta-Antagonists/pharmacology , Animals , Antihypertensive Agents/pharmacology , Calcium Channel Blockers/pharmacology , In Vitro Techniques , Prazosin/pharmacology , Propranolol/pharmacology , Rats , Rats, Wistar , Vasodilator Agents , Verapamil/pharmacologyABSTRACT
The experiments done on the isolated right ventricle of rat heart suspended in the bath for isolated organs with oxygenated Tyrode's solution showed the PgI2 (2.3 x 10-6 mmol) produced its positive inotropic effect indirectly by promoting both beta-adrenoreceptors and calcium entry through slow calcium channels because this effect could be blocked by propranolol (2.3 x 10-2 mmol - beta-adrenoreceptor blocker) or verapamil (4.3 x 10-3 mmol - slow calcium channel blocker).
