Influence of extracellular Ca2+ on the modulation of alpha-adrenergic-induced contractions in rat aorta.

1. Rat thoracic aortic rings with and without endothelium incubated in a Ca2(+)-free solution showed a significant reduction of the maximal contraction (E max) induced by norepinephrine (NE) and phenylephrine (Ph), while the contraction induced by a 70 mM KCl depolarizing solution was completely abolished. 2. After Ca2+ removal, pD2 values (-log ED50) for NE and Ph were significantly reduced only in vessels without endothelium. 3. Under control conditions, clonidine (C) induced a contraction only in vessels without endothelium; this response was completely abolished by Ca2+ removal and by nifedipine (10(-8) M). 4. Pre-incubation with nifedipine (10(-8) M) produced an effect similar, although less pronounced, than the removal of Ca2+ in vessels with and without endothelium. 5. Nevertheless, aortic rings with intact endothelium showed a greater reduction of E max than rings without endothelium, suggesting that the endothelial layer may act in synergism with calcium channel blockers to inhibit the contractions induced by alpha-adrenergic agonists. 6. The modulation exerted by the endothelium on alpha 1- and alpha 2-adrenergic-induced contractions in rat aortic rings seems to depend both on extracellular Ca2+ concentration and on the release and action of endothelial relaxing factor(s).