Characterization of Contractile Response to Angiotensin in Epididymal Rat Vas deferens

Angiotensin had a dual action on the epididymal half of rat vas deferens. It potentiated electrical stimulated contraction and exerted a direct contractile effect on the muscle. The potentiation of electrically stimulated response may be mediated by presynaptic facilitation of neurotransmitter release. Muscular contractile response to angiotensin is concentration dependent. Angiotensin II was found to be much more potent than angiotensin III, and the order of potencies was angiotensin II > angiotensin I > angiotensin III. The presence of a mixture of protease inhibitors (10 µM chymostatin, 50 µM bacitracin, 10 µM leupeptin and 10 µM pepstatin) did not alter the contractile activity of angiotensin II. In contrast, angiotensin I (10 nM)-induced contraction was significantly reduced in the presence of ACE inhibitor SQ 20881 (500 nM). The angiotensin II induced contraction was not reduced by CGP 42112, a specific AT₂ receptor antagonist, but was significantly inhibited by losartan, a specific ATi receptor antagonist. Losartan shifted the dose-response curve of angiotensin II to the right with a pA₂ value of 8.68. In addition, p-aminophenylalanine6 angiotensin II, which is proposed as an AT₂ receptor agonist, did not induce contraction. It is concluded that the AT₁ receptor predominantly mediates angiotensin-induced contraction in epididymal rat vas deferens.