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.
Morishita
H
H
Department of Pharmacology, School of Medicine, Fukuoka University, Japan.
Sakamoto
Y
Y
Furukawa
T
T
D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D000242:Cyclic AMP / Q000502:physiology*; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects* / Q000294:innervation; D011188:Potassium / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D000242:Cyclic AMP; D011188:Potassium; D002118:Calcium