CHARACTERIZATION OF CONTRACTILE RESPONSE TO ANGIOTENSIN IN EPIDIDYMALRAT VAS-DEFERENS

Angiotensin had a dual action on the epididymal half of rat vas defere ns. It potentiated electrical stimulated contraction and exerted a dir ect contractile effect on the muscle. The potentiation of electrically stimulated response may be mediated by presynaptic facilitation of ne urotransmitter release, Muscular contractile response to angiotensin i s concentration dependent. Angiotensin II was found to be much more po tent than angiotensin III, and the order of potencies was angiotensin II > angiotensin I > angiotensin III. The presence of a mixture of pro tease inhibitors (10 mu M chymostatin, 50 mu M bacitracin, 10 mu M leu peptin and 10 mu M pepstatin) did not alter the contractile activity o f angiotensin II. In contrast, angiotensin I (10 nM)-induced contracti on was significantly reduced in the presence of ACE inhibitor SQ 20881 (500 nM). The angiotensin II induced contraction was not reduced by C GP 42112, a specific AT(2) receptor antagonist, but was significantly inhibited by losartan, a specific AT(1) receptor antagonist. Losartan shifted the dose-response curve of angiotensin II to the right with a pA(2) value of 8.68. In addition, p-aminophenylalanine(6) angiotensin II, which is proposed as an AT(2) receptor agonist, did not induce con traction. It is concluded that the AT(1) receptor predominantly mediat es angiotensin-induced contraction in epididymal rat vas deferens.