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Objective: To study cross-talk between p-opioid receptor and β-adrenoceptor through determination of the intracellular calcium ( [ Ca2+ ]i ) and cAMP responses in ventricular myocytes of rats subjected to chronic hypoxia for 4 weeks. Methods: Electrically-induced [ Ca2+ ]i transient was measured in single right ventricular myocytes isolated from hearts of chronically hypoxic rats and the age-matched normoxic rats, by using a spectrofluorometric method. Results: β-adrenoceptor stimulation with isoproterenol increased the electrically-induced [ Ca + ]i transient and cAMP in myocytes of normoxic rats. U50,488H, a selective β-opioid receptor agonist, at dose (1 βmol/L) which itself had no effect on the [Ca2 + ]i transient and cAMP, significantly inhibited the effect of isoproterenol. This inhibition was completely abolished in the presence of nor-BNI, a selective K-opioid receptor antagonist. In the ventricular myocytes of chronically hypoxic rats, the inhibition of U50,488H on the increased [ Ca ]i tra
Objective: To study cross-talk between p-opioid receptor and β-adrenoceptor through determination of the intracellular calcium ([Ca2 +] i) and cAMP responses in ventricular myocytes of rats subjected to chronic hypoxia for 4 weeks. Methods: Electrically-induced [ Ca2 +] i transient was measured in single right ventricular myocytes isolated from hearts of chronically hypoxic rats and the age-matched normoxic rats, by using a spectrofluorometric method. Results: β-adrenoceptor stimulation with isoproterenol increased the electrically-induced [Ca +] i transient and cAMP in myocytes of normoxic rats. U50,488H, a selective β-opioid receptor agonist, at dose (1 βmol / L) which itself had no effect on the [Ca2 +] i transient and cAMP, significantly inhibited the effect of isoproterenol. This inhibition was completely abolished in the presence of nor-BNI, a selective K-opioid receptor antagonist. In the ventricular myocytes of chronically hypoxic rats, the inhibition of U50,488H on the inc reased [Ca] i tra