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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 microM chymostatin, 50 microM bacitracin, 10 microM leupeptin and 10 microM 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 AT1 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.

The effect of chronic caffeine treatment on lipolysis in rat epididymal adipose tissue was studied. There was a decrease in body weight, epididymal fat pad weight and mean adipocyte diameter in caffeine-treated rats when compared with control rats. No difference in adipocyte triglyceride content or mean adipocyte weight between control and caffeine-treated rats was observed. Lipolysis in adipocytes induced by adenosine deaminase (1 U/ml) decreased by 35% in caffeine-treated rats. This was accompanied by a 2.5-fold increase in the anti-lipolytic potency of 2-chloroadenosine and an increase of adipocyte adenosine A1 receptor number.