Potassium chloride (K+) produced dose-dependent contractions of the rat isolated seminal vesicle with no sign of tachyphylaxis. The contractile response was biphasic in nature and composed of an early rapid phasic contraction and a slowly developing, but more sustained, tonic response separated by a transient relaxation. Neither cocaine nor depletion of tissue catecholamines by reserpine influenced responses to K+. Moreover, guanethidine, phentolamine, phenoxybenzamine, atropine and physostigmine all failed to modify responses of the tissue to K+. Thus, the possibility of K+ acting via release of endogenous noradrenaline or acetylcholine is excluded. Calcium-free conditions with or without EGTA reduced both the components of K(+)-induced contraction. The rate of reduction of both responses was faster in the presence of EGTA with part of the tonic response being resistant even to calcium deprivation in the presence of EGTA. On the other hand, verapamil reduced both responses in a similar manner, whereas nifedipine produced dose-dependent rightward shifts of the concentration-response curves of both the phasic 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 rat seminal vesicle use extracellular Ca2+, of which some is tightly bound with high affinity, probably to plasma membranes. In addition, two subtypes of voltage-sensitive Ca2+ channels may exist, one of which is preferentially sensitive to nifedipine and both are sensitive to verapamil.