Involvement of calcium and cyclic AMP in the K+-induced rhythmic contraction of isolated rat vas deferens.

Mechanisms involved in the K+-induced rhythmic contraction were investigated in the isolated rat vas deferens. Isolated vas deferens is mechanically quiescent in normal Krebs-bicarbonate solution, but addition of KCl (10 to 35 mM) to the solution induces a rhythmic contraction. The K+-induced rhythmic contraction was not inhibited by tetrodotoxin, prazosin and indomethacin as well as by in vivo pretreatment with reserpine, but was abolished by verapamil or by Ca++ removal from the solution. TMB-8, a calcium release blocker, blocked the K+-induced rhythmic contraction and, instead, sustained tonic contractions developed. The rhythmic contraction was abolished by isoproterenol or by 3-isobutyl-1-methylxanthine, a phosphodiesterase inhibitor. The action of isoproterenol was inhibited by propranolol and was potentiated by 3-isobutyl-1-methylxanthine. In addition, dibutyryl cyclic AMP, but not dibutyryl C-GMP, blocked the rhythmic contraction. After those drugs affecting intracellular C-AMP levels, addition of excess KCl to the solution induced a sustained contraction, but not the rhythmic contraction. These results suggest that K+-induced rhythmic contractions are myogenic in origin and are caused by Ca++ movements which are controlled by intracellular cyclic AMP levels.