Calcium translocation during activation of alpha 1-adrenoceptor and voltage-operated channels in smooth muscle cells.

Changes in potential and mechanical activity were measured with the sucrose-gap method and changes in intracellular free calcium were determined from the fluorescence intensity of the calcium-quin 2 complex at 37 degrees C in smooth muscle cells of guinea-pig taenia caecum following alpha 1-adrenoceptor stimulation. The muscle cells responded with a transient hyperpolarization and a transient increase in intracellular free calcium on alpha 1-adrenoceptor stimulation in the absence of extracellular calcium. Sustained hyperpolarization, cessation of spike activity, relaxation and an increase in fluorescence intensity were observed following alpha 1-adrenoceptor stimulation in the presence of extracellular calcium. Similar characteristics were observed on alpha 1-adrenoceptor stimulation in the presence of diltiazem used to suppress spontaneous activity and in the presence of cytochalasin B used to prevent changes in the contractile state of the muscle cells. Treatment of the preparation with caffeine caused an initial depolarization, contraction and increase in free intracellular calcium. Stimulation of the alpha 1-adrenoceptors in the presence of caffeine did not block the alpha 1-adrenoceptor-induced hyperpolarization, but the changes in fluorescence intensity were completely inhibited. It was concluded from the results obtained that changes in intracellular calcium derived from both receptor and from voltage-operated systems were detected. Furthermore, it was concluded that mobilization of calcium, most likely from a plasma membrane-bound store, on alpha 1-adrenoceptor stimulation mediated the release of calcium from an intracellular compartment, probably the endoplasmic reticulum, and promoted the opening of potassium channels with as a result hyperpolarization and inhibition of smooth muscle activity of taenia caecum.(ABSTRACT TRUNCATED AT 250 WORDS)