Calcium fluxes in isolated rabbit aorta and guinea pig tenia coli.

Studies utilizing 45Ca have been helpful in analyzing the Ca control system in smooth muscle. Activation of rabbit aortic alpha receptors stimulates Ca influx and a release of Ca from superficial binding sites. Membrane depolarization by high K causes an influx, but no release. However, the influx pathways activated by alpha agonists and membrane depolarization are different and independent, because the maximal Ca influxes induced by each type of stimulation are additive. The cellular Ca pools that release Ca during pharmacological activation are shared by several agonists; release of cellular Ca by one agent after abolition of Ca influx inhibits Ca release by a second, different agonist. U44069, a stable prostaglandin H2 analog, induces both Ca influx and release. The extracellular Ca source for initial influx exchanges more slowly than free interstitial Ca, and may be located within the glycocalyx or on the outer membrane surface. An Na-Ca exchange process has been suggested as the important determinant of the transmembrane electrochemical Ca gradient. However, manipulation of the Na gradient by Na pump inhibition and Na substitution has provided data showing that Na-Ca exchange is a nonspecific process not directly involved in regulating [Ca]i. It is more likely that Ca extrusion is dependent on an ATPase in smooth muscle.