MECHANISMS INVOLVED IN ELECTRICALLY-INDUCED RESPONSES OF RAT SEMINAL-VESICLES

Contractile responses of rat isolated seminal vesicle were elicited by electrical field stimulation (EFS, 10 Hz, 1 ms, 40 V for 5 s), noradr enaline (1 x 10(-5) M) and carbachol (1 x 10(-5) M). Guanethidine (2 x 10(-5)-5 x 10(-4)M) progressively reduced the contraction induced by EFS and carbachol to 24 +/- 2 and 10 +/- 2%, respectively, at the high est concentration (n = 6), while potentiating noradrenaline contractio n to a maximum of 154 +/- 14% at 2 x 10(-5) M (n = 6). Prazosin (1 x 1 0(-6) M) and atropine(2.5 x 10(-7) M) completely abolished the respons e 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 n ot induce a contractile response and had an inhibitory effect on EFS-i nduced responses. Clonidine (1.25 x 10(-5) M) completely blocked respo nses 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 r emaining response to EFS (323 +/- 82%, n = 4). Yohimbine (1 x 10(-5) M ) blocked the response to noradrenaline and reduced the response to EF S to 37 +/- 5% (n = 6) while the carbachol response was unaffected. Bo th cholinergic and noradrenergic components contribute to the response to EFS but there appears to be little involvement of presynaptic alph a(2)-adrenoceptors in regulating neurotransmitter release. The actions of clonidine and yohimbine are compatible with the suggestion that th eir effects are due to postsynaptic alpha(1)-adrenoceptor blockade.