Stimulus secretion coupling in cultured chromaffin cells. Dependency on external sodium and on dihydropyridine-sensitive calcium channels

Abstract

Stimulus secretion in response to acetylcholine (or nicotine) in adrenal chromaffin cells involves calcium influx and is tetrodotoxin insensitive. The mechanism by which activation of the nicotinic acetylcholine receptor (AChR) leads to calcium influx is not clear, and the requirement for external sodium is controversial. We report that when bovine chromaffin cells are continuously perfused in the absence of sodium, secretion of catecholamines in response to 3 X 10(-5) M nicotine is not impaired. Also, secretion stimulated by this concentration of nicotine is not potently and stereospecifically inhibited by the (+)- and (-)-isomers of nicardipine. At a concentration of (+)-nicardipine (10(-7) M) which inhibits most of the release stimulated by 50 mM potassium, the response to 3 X 10(-5) M nicotine remains; however, the dose-response curve to nicotine is shifted slightly to the left. The results are discussed with respect to models of stimulus secretion coupling in bovine adrenal chromaffin cells.