Pharmacological characteristics of receptor-operated and potential-operated Ca2+ channels in rat aorta

In the rat aorta activation of the potential-operated Ca2+ channels by 100 mM K+ resulted in a greater 45Ca2+ influx than stimulation of the receptor-operated Ca2+ channels by norepinephrine (NE, 3 X 10(-7) M) or angiotensin II (AII, 10(-7) M). 45Ca2+ influx induced by NE was inhibited by prazosin (10(-7) M) but not by yohimbine (10(-6) M) while that by AII was abolished by [Sar1, Ile8]AII (10(-8) M). These receptor antagonists had no effect on the 45Ca2+ influx produced by K+. Bay k 8644 enhanced the influxes to low concentrations of NE and K+ while it was additive with the maximal concentration of NE but not with K+. 3-Isobutyl-1-methyl-xanthine and forskolin inhibited both the influx and efflux of 45Ca2+ elicited by NE but were ineffective against those caused by K+. Nifedipine blocked the efflux of 45Ca2+ induced by K+ but not that evoked by NE. However, both types of Ca2+ channel exhibited the same sensitivity to inhibition by Ca2+ entry blockers (nifedipine/verapamil) on 45Ca2+ influxes. These data suggest that in the rat aorta, the receptor-operated calcium channels and potential-operated calcium channels share similar structural characteristics. However, they are gated separately and distinctly by their respective activators.