Mechanisms Involved in Electrically-induced Responses of Rat Seminal Vesicles

Abstract

Abstract Contractile responses of rat isolated seminal vesicle were elicited by electrical field stimulation (EFS, 10 Hz, 1 ms, 40 V for 5 s), noradrenaline (1 times 10−5 m) and carbachol (1 times 10−5 m). Guanethidine (2 times 10−5−5 times 10−4 m) progressively reduced the contraction induced by EFS and carbachol to 24 ± 2 and 10 ± 2%, respectively, at the highest concentration (n = 6), while potentiating noradrenaline contraction to a maximum of 154 ± 14% at 2 times 10−5 m (n = 6). Prazosin (1 times 10−6 m) and atropine (2·5 times 10−7 m) completely abolished the response to the corresponding agonist and each reduced the response to EFS to 64 ± 8 and 61 ± 3%, respectively (n = 6). In the presence of both atropine and prazosin a small contraction to EFS remained (14 ± 4%, n = 6), which is unlikely to be due to ATP, since exogenous ATP did not induce a contractile response and had an inhibitory effect on EFS-induced responses. Clonidine (1·25 times 10−5 m) completely blocked responses to noradrenaline and reduced the response to EFS to 68 ± 7% (n = 6). However, when both the adrenergic and cholinergic components of EFS were blocked by prazosin and atropine, clonidine potentiated the remaining response to EFS (323 ± 82%, n = 4). Yohimbine (1 times 10−5 m) blocked the response to noradrenaline and reduced the response to EFS to 37 ± 5% (n = 6) while the carbachol response was unaffected. Both cholinergic and noradrenergic components contribute to the response to EFS but there appears to be little involvement of presynaptic α2-adrenoceptors in regulating neurotransmitter release. The actions of clonidine and yohimbine are compatible with the suggestion that their effects are due to postsynaptic α1-adrenoceptor blockade.