Interaction between neuropeptide Y Y1 receptors and α1B-adrenoceptors in the neurovascular junction of canine splenic arteries

Abstract Previous study has demonstrated that periarterial electrical nerve stimulation (30-s trains of pulses at a frequency of 1 or 4 Hz) induces a double-peaked vasoconstriction consisting of an initial transient, predominantly P2X-receptor-mediated constriction followed by a prolonged, mainly α 1 -adrenoceptor-mediated response in the isolated canine splenic artery. Treatment with 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY 7378, 0.1 μmol/l), a selective α 1D -adrenoceptor antagonist, produced a slight but significant inhibition of the second peaked responses. A marked inhibition of second peaked responses was obtained by exposure of the tissues to chloroethylclonidine (60 μmol/l), an α 1B - and α 1D -adrenoeptor antagonist. Neither BMY 7378 nor chloroethylclonidine affected the first peaked vasoconstrictor responses. [Leu 31 ,Pro 34 ]Neuropeptide Y (10–30 nmol/l), a selective neuropeptide Y Y 1 receptor agonist, enhanced the second peaked responses in the presence of BMY 7378 but failed to enhance the responses in the presence of chloroethylclonidine. The results indicate that the postjunctional α 1B -adrenoceptor subtype is likely coupled to neuropeptide Y Y 1 receptors responsible for the cooperation of the sympathetic adrenergic and neuropeptide Yergic transmission in the canine splenic artery.