The inhibitory effect of opioid and alpha 2-adrenoceptor agonists on cardiac sensory neurones is pertussis toxin-insensitive.

The role of pertussis toxin-sensitive G proteins on the alpha 2-adrenoceptor and mu-opioid receptor-mediated inhibition of the efferent function of capsaicin-sensitive neurones was investigated in guinea-pig atria pretreated with guanethidine. In the presence of atropine, CGP 20712A (2-hydroxy-5-(2-[hydroxy-3-(4-[(1-methyl- 4-trifluormethyl)1H-imidazol-2-yl]-phenoxy)propyl]aminoethoxyl+ ++)-benzamide) and prazosin, [D-Ala2,NMe-Phe4,Gly5-ol]enkephalin (DAGO, 0.1-3 microM) and 2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo(4,5-d)azepine (BHT 920, 0.01-1 microM) reduced the positive inotropic effect induced by transmural stimulation of preparations obtained from control and from pertussis toxin-treated animals. These results suggest that pertussis toxin-sensitive G proteins are not involved in the inhibitory regulation of the efferent function of capsaicin-sensitive nerve terminals in cardiac tissue induced by alpha 2 and opioid receptor stimulation.