Mechanisms of inhibitory noradrenergic transmission in the rabbit facial vein.

In isolated buccal segment of the rabbit facial vein, electrical responses produced by perivascular nerve stimulation and exogenously applied noradrenaline (NA) were recorded from the smooth muscle cells using microelectrode. Perivascular nerve stimulation hyperpolarized the smooth muscle cell membrane. The hyperpolarization was converted to depolarization after application of the beta-adrenoceptor antagonist, propranolol, and the depolarization was blocked by alpha 2-adrenoceptor antagonists, yohimbine. These responses elicited by nerve stimulation were blocked by tetrodotoxin or guanethidine, but not by atropine. Exogenously applied NA mimicked the responses elicited by nerve stimulation. The amplitude of the beta-adrenoceptor-mediated hyperpolarization was increased in low potassium solution, decreased in high potassium solution, but unaltered by low sodium or low chloride solution, i.e., the hyperpolarization may be generated by an increase in potassium conductance of the membrane. An involvement of the apamin-sensitive (Ca-dependent) potassium channel or sodium-potassium ATPase in the hyperpolarization was ruled out.