KC1 CONTRACTIONS IN THE RAT ISOLATED SEMINAL-VESICLE

Potassium chloride (K+) produced dose-dependent contractions of the ra t isolated seminal vesicle with no sign of tachyphylaxis. The contract ile response was biphasic in nature and composed of an early rapid pha sic contraction and a slowly developing, but more sustained, tonic res ponse separated by a transient relaxation. Neither cocaine nor depleti on of tissue catecholamines by reserpine influenced responses to K+. M oreover, guanethidine, phentolamine, phenoxybenzamine, atropine and ph ysostigmine all failed to modify responses of the tissue to K+. Thus, the possibility of K+ acting via release of endogenous noradrenaline o r acetylcholine is excluded. Calcium-free conditions with or without E GTA reduced both the components of K+-induced contraction. The rate of reduction of both responses was faster in the presence of EGTA with p art of the tonic response being resistant even to calcium deprivation in the presence of EGTA. On the other hand, verapamil reduced both res ponses in a similar manner, whereas nifedipine produced dose-dependent rightward shifts of the concentration-response curves of both the pha sic and tonic responses to K+. However, in the presence of nifedipine, the maximum response of only the phasic contraction was significantly lowered. It is concluded that both phases of KCl contraction in the r at seminal vesicle use extracellular Ca2+, of which some is tightly bo und with high affinity, probably to plasma membranes. In addition, two subtypes of voltage-sensitive Ca2+ channels may exist, one of which i s preferentially sensitive to nifedipine and both are sensitive to ver apamil.