Differences in norepinephrine activation and diltiazem inhibition of calcium channels in isolated rabbit aorta and mesenteric resistance vessels.

Abstract

The mechanisms of norepinephrine stimulation of calcium ion entry in isolated rabbit aorta and mesenteric resistance vessels were studied through measurements of effects on calcium-45 influx, tension, and membrane potential. The resistance vessels were considerably less sensitive to norepinephrine than the aorta. The aorta exhibited complex dose-response curves for norepinephrine-stimulated calcium influx and contraction, whereas these were simple in the arterioles. Both vessels were depolarized with increasing concentrations of potassium. Norepinephrine did not depolarize the aorta, whereas it did depolarize the mesenteric resistance vessels. This result supports the contention that norepinephrine opens receptor-operated channels to induce calcium entry in the aorta, while it may activate potential sensitive calcium channels in the mesenteric resistance vessels. However, the maximum depolarization with norepinephrine (10(-4) M) in the arterioles was completely blocked by 10(-5) M diltiazem, whereas that induced by 80 mM potassium was unaltered by the diltiazem. Furthermore, 10(-4) M norepinephrine was able to stimulate virtually the same contraction and calcium influx in 80 mM potassium-depolarized arterioles as in normal polarized tissues. These results are consistent with norepinephrine opening of receptor-operated channels to allow calcium entry in the rabbit mesenteric resistance vessels. That the behavior of norepinephrine-activated channels in the aorta is more complex than in the arterioles is further illustrated by a dramatically decreasing sensitivity of norepinephrine-stimulated calcium influx to diltiazem with increasing norepinephrine in the aorta but not in the arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Single nisoldipine-sensitive calcium channels in smooth muscle cells isolated from rabbit mesenteric artery.

“…Depolarizing voltage steps to -25 mV further increased the percentage of pulses that activated channels to -50%. Thus, the voltage sensitive range of these channels is within the physiological range of those membrane potentials that initiate Ca influx and cellular contraction (14,15). Proc.…”

“…Single channel recordings were accomplished using the patch-clamp technique as described by Hamill et al (10); the patch pipettes (Boralex, Rochester Scientific, Rochester, NY) with resistances of [10][11][12][13][14][15][16][17][18][19][20] MfQ were made with a vertical puller (David Kopf, Tujunga, CA; model 700C). After positioning the patch pipette against the cell, a high resistance seal (1-20 GQl) formed spontaneously.…”

The Effect of Vitamin A on Contraction of the Ductus Arteriosus in Fetal Rat

“…Measurement of the intracellular Ca pool using norepinephrine was performed to determine whether vitamin A treatment alters its size. It must be noted that norepinephrine stimulates not only alpha-adrenergic receptors, but also beta-receptors and increases Ca influx via Ca channels (15)(16)(17). To eliminate the Ca influx via the Ca channel, the effect of norepinephrine was examined in the absence of extracellular Ca (16).…”

“…In some experiments, the indomethacin concentration was increased to 3 ϫ 10 -6 M. The size of the intracellular Ca pool was examined using norepinephrine. Norepinephrine increases Ca influx via Ca channels by stimulating beta-receptors, and releases Ca from intracellular store sites by stimulating alpha-receptors (15)(16)(17). To eliminate the Ca influx via the Ca channel and Ca efflux via Na-Ca exchange, the effect of norepinephrine was examined in the absence of extracellular Na and Ca (16).…”

“…To induce membrane depolarization, high K was used and the effect of high KCl on ductal contraction and [Ca] i was measured. The size of the intracellular Ca pool was examined using norepinephrine, which releases Ca from intracellular store sites (15)(16)(17).…”