Abstract
The role of pertussis toxin-sensitive G proteins on the α 2-adrenoceptor and μ-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-Ala 2,NMe-Phe 4,Gly 5-ol]enkephalin (DAGO, 0.1−3 μM) and 2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo(4,5-d)azepine (BHT 920, 0.001−1 μM) 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 α 2 and opioid receptor stimulation.
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