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Potentiation of purinergic transmission by angiotensin in prostatic rat vas deferens
Author(s) -
Sum ChiShing,
Wan David C.C.,
Cheung WingTai
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15569.x
Subject(s) - vas deferens , endocrinology , medicine , purinergic receptor , angiotensin ii , losartan , carbachol , stimulation , reserpine , chemistry , antagonist , biology , receptor
1 Angiotensin II (AII) elicited only a minute, if any, direct contractile response in smooth muscle cells of prostatic rat vas deferens, but it potentiated contractile responses to field stimulation. 2 Angiotensin‐potentiated contractile response to field stimulation was concentration‐dependent, and the order of potency was AII > AIII ≅ AI. The EC 50 of AII was 8.11 ± 2.79 nM. 3 AII did not modify the contractile response of exogenous noradrenaline (NA) on non‐stimulated prostatic vas deferens. Furthermore, the concentration‐response curve for AII‐potentiated contractile responses to field stimulation in reserpine‐treated rats did not significantly differ from the control group. 4 Desensitization of purinoceptors with 30 μ m α, β‐methylene‐ATP almost completely abolished the potentiation of the contractile response to field stimulation by AII. 5 The response to AII in the prostatic rat vas deferens was blocked by the AT 1 selective antagonist losartan, but not by the AT 2 selective antagonist CGP 42112. Losartan acted as a competitive antagonist with a pA 2 value of 8.75. 6 In conclusion, AII potentiated purinergic transmission in the prostatic rat vas deferens via the AT 1 receptor.