EFFECT OF MODERATE COOLING ON CONTRACTILE RESPONSES IN MOUSE VAS-DEFERENS AND ITS RELATION TO CALCIUM

Isolated mouse vas deferens preparations were used to study the effect of temperature on noradrenaline-induced contractions. Preparations we re suspended in the organ bath containing Krebs-Henseleit solution for isometric tension recording. Contractile responses to noradrenaline w ere investigated in the mouse vas deferens after moderate cooling from 37 to 26 or 22 degrees C. A significant increase of the phasic contra ctions to noradrenaline was observed at 26 or 22 degrees C compared wi th responses obtained at 37 degrees C (about 12.3 and 35.6% increase a t 26 and 22 degrees C, respectively). The secondary noradrenaline-indu ced sustained contraction was also significantly enhanced after modera te cooling to 26 degrees C. The potentiation of noradrenaline-induced contraction at 26 degrees C remained in a Ca2+-free EGTA (1 mM)-contai ning solution. However, sustained contraction was suppressed after rem oval of the calcium from the medium at 37 and 26 degrees C. Contractio n to caffeine was significantly enhanced at 22 degrees C compared with 37 degrees C. By contrast, barium chloride-induced contraction of the vas deferens was markedly decreased after moderate cooling to 22 degr ees C. In the presence of ouabain (0.1 mM), the noradrenaline-induced peak contraction was significantly increased at 37 degrees C. However, potentiation of the noradrenaline response at 22 degrees C was unaffe cted by the Na+/K+ pump inhibitor. Noradrenaline-induced peak contract ions were depressed in the presence of vanadate (1 mM) and cyclopiazon ic acid (10 mu M), two Ca2+-ATPase inhibitors, at 37 degrees C and als o at 22 degrees C. These results suggest that temperature-induced hype rreactivity is partly due to an increase of the amount of calcium rele ased from intracellular stores. The inhibition of the Na+/K+ pump due to cooling may participate in this effect whereas Ca2+-ATPase inhibiti on does not seem to be involved.