Effect of calcium withdrawal and agents affecting calcium translocation on agonist-induced contractions of the rabbit ovarian artery.

The effect of extracellular calcium ion (Ca2+) depletion, diltiazem, D-600 and TMB-8 on potassium (K+), norepinephrine-(NE) and histamine-induced contractions of the rabbit isolated ovarian artery was studied. K+-induced contractions, which were biphasic, were rapidly lost (congruent to 5 min) when calcium was removed from the physiological saline solution (O-Ca2+ PSS). NE and histamine-induced contractions also declined rapidly under nominal O-Ca2+ conditions without any evidence of a depletion resistant component. However, after 1 h under these conditions there was a partial restoration of their responses. EGTA (10(-3) mol/l) abolished these contractions to NE and histamine but not those in normal PSS. Diltiazem and D-600 were more effective against K+-induced than NE- and histamine-induced contractions while the intracellular Ca2+ antagonist TMB-8 was equally effective against all three responses. Histamine could still evoke contraction of the K+-contracted ovarian artery after this had been completely abolished with diltiazem or D-600 but not TMB-8. These results are interpreted to suggest that K+, NE and histamine probably release intracellular Ca2+ to evoke contractions of the ovarian artery. They differ, however, in the mechanisms they employ to facilitate entry of extracellular calcium, which in turn leads to intracellular calcium release.