Abstract
Minute pieces of rat parotid gland were used in studies of adrenergic regulation of K+ efflux using86Rb+ as a probe for K+. Noradrenaline induced a concentration‐dependent Rb+ efflux, whereas the β1‐selective agonist prenalterol was without effect. On the other hand, the β2‐selective drug, terbutaline, at high concentrations displayed a small enhancement of Rb+ ‐secretion. The selective α1‐adrenoceptor drug, phenylephrine, was as potent as noradrenaline, whereas the α2‐agonist clonidine had only a small effect. The noradrenaline‐induced Rb+‐efflux was effectively inhibited in the presence of prazosin, an α1‐blocker, whereas the α2‐antagonist, yohimbine, was roughly 50 times less potent. The results suggest that catecholamine‐induced K+‐secretion from the rat parotid gland is mediated via activation of post‐synaptic α‐adrenoceptors of the α1‐subtype.