Pharmacological characterization of alpha-adrenoceptors involved in nictitating membrane and pupillary responses to sympathetic nerve stimulation in cats.

Electrical stimulation of the preganglionic cervical sympathetic nerve produced frequency-related contraction of the nictitating membrane (NM) and dilation of the pupil in anesthetized cats. Observations of the effects of alpha-adrenoceptor blockade on these effectors were made simultaneously from the same preparations. All of the alpha 1-adrenoceptor antagonists tested produced a dose-related blockade of the NM with the relative potencies being prazosin greater than WB-4101 greater than phentolamine greater than phenoxybenzamine. In contrast, the iris dilator response was blocked by WB-4101 and phenoxybenzamine but was almost totally refractory to antagonism by doses of prazosin and phentolamine that reduced the evoked NM responses by more than 75% in these same preparations. Neither alpha 2-adrenoceptor (yohimbine or rauwolscine) nor beta-adrenoceptor (propranolol) antagonism produced significant inhibition of the activation of either organ. These results suggest that: 1) neural activation of the nictitating membrane is solely due to stimulation of alpha 1-adrenoceptors; 2) neither beta- nor alpha 2-adrenoceptors contribute significantly to nerve activation of either the nictitating membrane or iris dilator muscle in vivo; 3) the alpha-adrenoceptors on the dilator muscle that are activated neurally can not be classified pharmacologically as either alpha 1 or alpha 2 receptors.