Mechanisms involved in electrically-induced responses of rat seminal vesicles
Sadraei, H.; Large, B.J.; Hughes, I.E.
Journal of Pharmacy and Pharmacology 47(8): 665-668
1995
ISSN/ISBN: 0022-3573 PMID: 8583369 Document Number: 448746
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 add 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 alpha-2-adrenoceptors in regulating neurotransmitter release. The actions of clonidine and yohimbine are compatible with the suggestion that their effects are due to postsynaptic alpha-1-adrenoceptor blockade.