Nicotine-evoked cytosolic Ca(2+) increase and cell depolarization in capillary endothelial cells of the bovine adrenal medulla.

Endothelial cells are directly involved in many functions of the cardiovascular system by regulating blood flow and blood pressure through Ca(2+) dependent exocitosis of vasoactive compounds. Using the Ca(2+) indicator Fluo-3 and the patch-clamp technique, we show that bovine adrenal medulla capillary endothelial cells (B AMCECs) respond to acetylcholine (ACh) with a cytosolic Ca(2+) increase and depolarization of the membrane potential (20.3+/-0.9 mV; n=23). The increase in cytosolic Ca(2+) induced by 10microM ACh was mimicked by the same concentration of nicotine but not by muscarine and was blocked by 100 microM of hexamethonium. On the other hand, the increase in cytosolic Ca(2+) could be depressed by nifedipine (0.01 -100 microM) or withdrawal of extracellular Ca(2+). Taken together, these results give evidence for functional nicotinic receptors (nAChRs) in capillary endothelial cells of the adrenal medulla. It suggests that nAChRs in B AMCECs may be involved in the regulation of the adrenal gland's microcirculation by depolarizing the membrane potential, leading to the opening of voltage-activated Ca(2+) channels, influx of external Ca(2+) and liberation of vasoactive compounds.