α-Adrenoceptor activation of nictitating membrane and iris in cats

Summary

Intra-arterial administration of (+)- and (−)isomers of adrenaline and noradrenaline produced doserelated contraction of the nictitating membrane (NM) and dilation of the pupil in anesthetized cats. The relative potencies were (−)-adrenaline > (+)-adrenaline = (−)-noradrenaline > (+)-noradrenaline. Observations of the effects of α-adrenoceptor antagonists on (−)-noradrenaline activation of these two effectors were made simultaneously. All of the α₁-adrenoceptor antagonists tested produced a doserelated blockade of the NM with the relative potencies being prazosin > WB-4101 > phentolamine > phenoxybenzamine. In contrast, the iris dilator was blocked by WB-4101 and phenoxybenzamine but was refractory to antagonism by doses of prazosin and phentolamine that reduced the (−)-noradrenaline evoked NM response by 75–80% in the same animals. The α₂-adrenoceptor antagonist, yohimbine, produced significant inhibition of the NM only at high dose (1 mg/kg) but even at this level had no effect on pupil diameter. These results suggest that activation of the NM by exogenous noradrenaline is due solely to stimulation of α₁-adrenoceptors. α₂-adrenoceptors do not seem to significantly contribute to noradrenaline induced activation of either the NM or iris dilator muscle in vivo. In contrast, the α-adrenoceptors on the iris dilator muscle that are stimulated by exogenous noradrenaline can not easily be classified pharmacologically as either α₁- or α₂-adrenoceptors.