Ca(2+) uptake function of sarcoplasmic reticulum during contraction of rat arterial smooth muscles.

To determine the Ca(2+) uptake function of the sarcoplasmic reticulum during contraction, the effects of cyclopiazonic acid or thapsigargin, agents that inhibit sarcoplasmic reticulum Ca(2+)-ATPase, on the contractile responses to K(+) or norepinephrine were compared in endothelium-denuded strips of femoral, mesenteric and carotid arteries of the rat. The addition of K(+) (3-20 mM) to the strips caused a concentration-dependent contraction, and the sensitivity to K(+) was much higher in the carotid artery than in the other arteries. The preincubation of strips with cyclopiazonic acid (10 microM) or thapsigargin (100 nM) caused a leftward shift of the concentration-response curve for K(+), and this effect was smaller in the carotid artery than in the other arteries. Inhibition of sarcoplasmic reticulum Ca(2+) uptake caused the sensitivity to K(+) to be similar in the three arteries. Similar results were obtained when the contractile responses to norepinephrine were determined. Cyclopiazonic acid itself induced similar transient contractions in the three arteries. The addition of caffeine (20 mM) caused a transient contraction that was smaller in the carotid artery than in the other arteries. We conclude that (1) the Ca(2+) influx during stimulation with K(+) or norepinephrine is buffered by the sarcoplasmic reticulum in femoral and mesenteric arteries, (2) this function is weak in the carotid artery, probably because the sarcoplasmic reticulum of this artery is almost filled with Ca(2+) in the resting state, and (3) the Ca(2+) uptake function of the sarcoplasmic reticulum during contraction is reflected by the contractile sensitivity in these arteries.