Vasoconstrictor responses of rat tail artery to sympathetic nerve stimulation contain a component due to activation of postjunctional beta- or alpha 2-adrenoceptors.

The role of alpha 1-, alpha 2- and beta-adrenoceptors in vasoconstrictor responses to sympathetic nerve stimulation was investigated in perfused proximal segments of rat tail artery by using selective blocking drugs. Prazosin (1 nM) markedly reduced the responses but idazoxan (100 nM) did not, and propranolol (1 microM) significantly enhanced them, indicating that the vasoconstriction was due to activation of alpha 1-adrenoceptors and that it was partly counteracted by a vasodilator component due to activation of beta-adrenoceptors. In the presence of propranolol, idazoxan or reduction of the concentration of Ca2+ in the perfusing solution from 2.5 to 0.63 mM significantly reduced responses to sympathetic nerve stimulation, indicating that a component of the vasoconstrictor response was due to activation of alpha 2-adrenoceptors. Forskolin, which increases cyclic AMP levels independently of beta-adrenoceptors, reduced responses to sympathetic nerve stimulation to a greater extent in the presence than in the absence of propranolol and this effect was additive with that of prazosin but not idazoxan. It is concluded that activation of beta-adrenoceptors inhibits the component of responses to sympathetic nerve stimulation due to activation of alpha 2-adrenoceptors because of an inhibitory effect of cyclic AMP on Ca2+ channels linked to alpha 2-adrenoceptors.