The effect of Ca deprivation and of Ca-blocking drugs on oxytocin-induced contractions of the male mouse anococcygeus.

Oxytocin (4 nM)-induced contractions of the male mouse anococcygeus were rapidly and completely lost in EGTA (2 mM)-containing, Ca-free Krebs solution. Contractions were also lost, although more slowly, in Ca-free Krebs solution without EGTA; under such conditions, readdition of Ca did not by itself cause contraction, but readdition of Ca (0.1-2.5 mM) in the presence of 4 nM oxytocin resulted in a rapid contractile response. These Ca-induced responses, in the presence of oxytocin, and those to oxytocin in normal Ca-containing Krebs solution, were unaffected by nitrendipine (0.01-1 microM). Contractions to oxytocin were completely blocked by the calmodulin antagonists trifluoperazine (50 microM) and W-7 (75 microM). It is concluded that oxytocin-induced contraction of the mouse anococcygeus does not require opening of nitrendipine-sensitive Ca channels, and there is no Ca-independent component of the contractile response; the cellular mechanisms linked to the oxytocin receptor in the anococcygeus are therefore different from those in the uterus.