CA2+ REMOVAL MECHANISMS IN RAT CEREBRAL RESISTANCE SIZE ARTERIES

Tissue blood flow and blood pressure are each regulated by the contrac tile behavior of resistance artery smooth muscle. Vascular diseases su ch as hypertension have also been attributed to changes in vascular sm ooth muscle function as a consequence of altered Ca2+ removal. In the present study of Ca2+ removal mechanisms, in dissociated single cells from resistance arteries using fura-2 microfluorimetry and voltage cla mp, Ca2+ uptake by the sarcoplasmic reticulum and extrusion by the Ca2 + pump in the cell membrane were demonstrably important in regulating Ca2+. In contrast, the Nac-Ca2+. exchanger played no detectable role i n clearing Ca2+. Thus a voltage pulse to 0 mV, from a holding potentia l of -70 mV, triggered a Ca2+ influx and increased intracellular Ca2concentration ([Ca2+](i)). On repolarization, [Ca2+](i) returned to th e resting level. The decline in [Ca2+](i) consisted of three phases. C a2+ removal was fast immediately after repolarization (first phase), t hen plateaued (second phase), and finally accelerated just before [Ca2 +](i) returned to resting levels (third phase). Thapsigargin or ryanod ine, which each inhibit Ca2+ uptake into stores, did not affect the fi rst but significantly inhibited the third phase. On the other hand, Na + replacement with choline(+) did not affect either the phasic feature s of Ca2+ removal or the absolute rate of its decline. Ca2+ removal wa s voltage-independent; holding the membrane potential at 120 mV, rathe r than at -70 mV, after the voltage pulse to 0 mV, did not attenuate C a2+ removal rate. These results suggest that Ca2+ pumps in the sarcopl asmic reticulum and the plasma membrane, but not the Na+-Ca2+ exchange r, are important in Ca2+ removal in cerebral resistance artery cells.