Previous studies have shown that norepinephrine (NE) and the beta-adrenoceptor agonist, isoproterenol (I), enhance fluid absorption (Jv) in isolated, perfused proximal convoluted tubule segments (PCT). Pretreatment of PCT with the beta-adrenoceptor antagonist, propranolol, inhibited the action of NE and produced a significant decline in Jv, suggesting modulation of Jv by both alpha- and beta-adrenoceptors. The present studies further characterize the alpha-adrenoceptor control of Jv in isolated perfused PCT using specific agonists and antagonists. Basal Jv declined significantly with the addition of the alpha2-adrenoceptor agonist, clonidine (10-4 M), to the bath; however, it was unchanged with the addition of the alpha1-adrenoceptor agonist, methoxamine (10-6 or 10-4 M). With the addition of 10-6 M isoproterenol Jv increased significantly, and returned to control values with the subsequent addition of clonidine (10-6 or 10-4 M). Pretreatment of PCT with the alpha2-adrenoceptor antagonist, yohimbine (10-5 M), or with pertussis toxin (100 ng/ml) did not interfere with the stimulation of Jv by isoproterenol, but abolished the inhibition of isoproterenol-stimulated Jv by clonidine. Thus, clonidine inhibits Jv in PCT via an alpha2-adrenoceptor. This effect is mediated by a pertussis toxin inhibitable GTP-binding protein, but not one that is coupled to adenylyl cyclase.
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