Sources of calcium used during alpha 1- and alpha 2-adrenergic contractions in canine saphenous veins.

Experiments were performed to determine the role of intra- and extracellular Ca2+ during contractions of canine saphenous veins evoked with 'alpha 1'- and 'alpha 2'-adrenergic agonists. After incubation in Ca2+-free medium for 45 min, noradrenaline, clonidine and phenylephrine caused contractions, reaching a maximal amplitude rapidly and then declining to a lower stable level within 6 min. The maximal amplitude amounted to about 10% of the response to the agonists in physiological saline containing Ca2+ ions. After a previous exposure to one of the alpha-adrenergic agonists in Ca2+-free medium, no peak response was observed when the preparations were exposed to any of the agonists a second time. The stable smaller contractions which followed the peak response could however be repeated after a previous exposure to one of the agonists. In normal physiological salt solution (PSS), iproveratril depressed the maximal response to all three agonists to about 60% of the control value. However, the shift of the median effective dose (ED50) to the right was larger for clonidine than for the other two agonists. Noradrenaline, clonidine and phenylephrine (all at 10(-5) M) increased the uptake of 45Ca. Iproveratril reduced this increased uptake of 45Ca. Noradrenaline, clonidine, guanfacine and phenylephrine augmented the efflux rate of 45Ca. After exposure to one of the agonists, noradrenaline caused no or only a moderate increase of the efflux rate of 45Ca. The present experiments indicate that in the dog's saphenous vein: (1) alpha 1- and alpha 2-adrenergic activation cause both influx of Ca2+ ions and release of intracellular Ca2+; (2) the source of the intracellular Ca2+ is the same; (3) the mechanism underlying the influx of extracellular Ca2+ ions into the smooth muscle cells, to judge from the inhibiting effect of iproveratril, is most likely to be the same.