Effects of thioridazine on mechanical responses of human vas deferens induced by noradrenaline or potassium

Abstract

Summary. Thioridazine (0\ m=. \ 1\ p=n-\ 10\g=m\moll \ m=-\ 1) inhibited shortening of specimens of human vasa deferentia induced by noradrenaline (100 \g=m\moll \ m=-\ 1 ) or high extracellular potassium (136 mmol l \ m=-\ 1). Thioridazine did not inhibit the lengthening response. In Ca2+ -free media with EGTA (0\m=.\5 mmol l \m=-\ 1) similar results were obtained with responses to noradrenaline, but exposure to potassium elicited small contractions that were potentiated by thioridazine. Both shortening and lengthening responses to noradrenaline were antagonized by the \g=a\-adrenoceptor blockers prazosin (1\p=n-\10\g=m\mol l \ m=-\ 1) and phentolamine (1\p=n-\10 \g=m\moll\m=-\1) and by the Ca2+ antagonists verapamil (10 \g=m\moll \ m=-\ 1) and diltiazem (10 \g=m\mol l \ m=-\ 1). Responses to potassium were virtually abolished by the Ca2+ antagonists.These results show that thioridazine specifically inhibits longitudinal muscle of the human vas deferens and that its action cannot be entirely accounted for by a blockade of voltage-gated Ca2+ channels.