• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.171-179
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• 1992

Effects of a $M_1$ receptor antagonist, pirenzepine, a $M_2$ receptor antagonist, AF-DX116, and a nicotinic receptor antagonist, mecamylamine on the pressor responses to preganglionic sympathetic nerve stimulation (PNS) and McN-A-343 and DMPP in spinal (pithed) rabbits were investigated, in order to elucidate a functional role of $M_1$, $M_2$ and nicotinic receptors in ganglionic transmission. Pirenzepine and AF-DX116 selectively inhibited the McN-A-343-induced pressor response in chlorisondamine-treated rabbit and the BCh-induced bradycardia, respectively. Electrical stimulations of preganglionic sympathetic outflow at T8 level produced increases in blood pressure. Pirenzepine $(3\;{\mu}g/kg)$ significantly inhibited the PNS-induced pressor response and the degree of inhibition was not changed by increasing the doses to $100\;{\mu}g/kg$. AF-DX116 $(100\;{\mu}g/kg)$ had no effect on the PNS-induced pressor response. Mecamylamine inhibited the PNS-induced pressor response in a dose-dependent manner. The inhibitory action of mecamylamine was significantly augmented by combined-treatment with pirenzepine $(30\;{\mu}g/kg)$ but AF-DX116 $(100\;{\mu}g/kg)$ did not affect the inhibitory action of mecamylamine. McN-A-343 and DMPP elicited pressor response in the spinal rabbit. Pirenzepine and AF-DX116 dose-dependently inhibited the McN-A-343-induced pressor response but they did not affect DMPP-induced pressor response. Mecamylamine inhibited both pressor responses induced by McN-A-343 and DMPP. These results suggest that not only nicotinic receptors but also $M_1$ receptors play a facilitatory role in ganglionic transmission but $M_2$ receptors do not contribute the transmission in spinal (pithed) rabbits.