Trachte G J
Department of Pharmacology, University of Minnesota-Duluth School of Medicine.
J Pharmacol Exp Ther. 1990 Apr;253(1):80-4.
Angiotensin II inhibits nonadrenergic (purinergic) neurotransmission in the vas deferens and potentiates adrenergic neurotransmission and prostaglandin (PG)E synthesis. Other angiotensin responses are sensitive to either dithiothreitol or pertussis toxin. The present study tested the hypothesis that dithiothreitol or pertussis toxin selectively depress angiotensin responses in the vas deferens. The dithiothreitol (10 mM) eliminated the potentiation of both adrenergic neurotransmission and PGE synthesis but did not alter the depression of purinergic neurotransmission. In contrast, pertussis toxin (100 ng/ml for 3 hr) eliminated the depression of purinergic neurotransmission but had no effect on adrenergic neurotransmission or PGE synthetic responses to angiotensin II. The results are consistent with the existence of at least two transduction pathways for angiotensin II, one enhancing adrenergic neurotransmission and PGE synthesis and the other depressing purinergic neurotransmission. The results indicate that the vas deferens is a useful preparation in defining selective actions of angiotensin receptor agonists or antagonists.
