Differential calcium dependence of contractile responses and 86Rb efflux from the rabbit aorta induced by vasoactive stimuli.

86Rb was used to monitor potassium movements in strips of rabbit aorta simultaneously with measurements of tension. Histamine, noradrenaline, the prostaglandin endoperoxide analogue U46619, angiotensin II, and 144 mM K+ each induced an increase in 86Rb efflux concomitantly with contraction. For the first four agonists there was a rank-order correlation between the contractile response and 86Rb efflux, but 144 mM K+ induced a massive increase in 86Rb efflux although it was the weakest contractile stimulus. Contraction and increase in 86Rb efflux-induced K+ were both reduced by verapamil, which blocks voltage-sensitive calcium channels, implying that both effects of K+ were mediated mainly by a depolarisation-induced influx of calcium. Noradrenaline increased both tension and 86Rb efflux through an action on alpha-adrenoceptors, but its effect on efflux, unlike its effect on tension, was apparently totally dependent on the presence of extracellular calcium. Experiments performed in the presence of lanthanum, which blocks calcium influx, showed that the intracellular store of calcium released by noradrenaline apparently played no role in inducing 86Rb efflux, although it could trigger contraction. Lanthanum also blocked contraction induced by K+ but had less effect on the increase in 86Rb efflux induced by K+. Thus, agonist-induced vascular contraction and 86Rb efflux can be dissociated, but under normal conditions all the contractile stimuli tested induced 86Rb efflux.