Alpha 2-agonists block ADH action in toad bladder and this inhibition is not modified by indomethacin.

To identify the type of alpha-adrenoceptors involved in the inhibition of the hydrosmotic effect of antidiuretic hormone (ADH) on the toad bladder, we studied the effect of different alpha-adrenergic agonists and antagonists on ADH-induced water transport. Serosal addition of epinephrine (10(-6) M) and norepinephrine (10(-6) M) in the presence of 10(-4) M propranolol significantly inhibited the hydrosmotic effect of ADH (arginine vasopressin). This inhibitory effect of the catecholamines was completely reversed by 10(-5) M yohimbine but not by prazosin. Clonidine did not block ADH-induced water transport, but guanabenz, another alpha 2-agonist, inhibited water transport in response to ADH. In bladders pretreated with indomethacin to block prostaglandin synthesis, basal water permeability was increased, and even in this condition epinephrine inhibited ADH-induced water transport. These studies indicate that alpha 2-adrenergic receptors are involved in the inhibitory effect of catecholamines on ADH-mediated water permeability in the toad bladder. However, this effect was not mimicked by clonidine, as in the case of rabbit cortical collecting tubule. The inhibitory effect of epinephrine appears to be exerted independently of prostaglandin synthesis.