Neuroscwnce Letters, 101 (1989) 101 106 101 Elsevier Scientific Pubhshers Ireland Ltd NSL 06116 Sodium-dependent and sodium-independent nicotine-evoked catecholamine release from cat adrenals F.J. Abajo, M.A.S. Castro, C.R. Lopo, B. Garijo, P. Sanchez-Garcia and A.G. Garcia Department of Pharmacology, UmversidadAutonoma de Madrid, Facultad de Medwma, Madrid (Spain) (Received 19 May 1988; Rvwsed version received 13 February 1989, Accepted 15 February 1989) Key words Catecholamme release; Adrenal medulla, Acetylchohne receptor, Calcmm channel Cat adrenal glands were samulated ruth mcotme under Na-free condmons, subsequently, Na was gra- dually introduced as a continuously increasing gradient from 0 to 134 mM With this expenmental ap- proach two catecholamme secretory peak responses were obtained one was Na-mdependent and the second was dependent of this cation This second response was greater in magnitude than the first and selectively blocked by (+)PN200-110, a potent dlhydroplndme Ca channel blocker. The results suggest that Na, although not essential to evoke some degree of secretion, plays, however, a prominent role m amphfymg the nicotine-secretory response by causing cell depolanzation and opening of voltage-de- pendent Ca channels To trigger acetylcholine-evoked catecholamine release [9], Ca ions might gain ac- cess to the adrenal chromaflin cell secretory machinery through voltage-dependent and nicotinic receptor-associated channels. However, the relative contribution of each channel type as well as the role of Na ions in secretion are still matters of contro- versy In the literature. While some authors conclude that the influx of Ca through voltage-dependent channels is the common ionic event in triggenng catecholamine release evoked either by K, veratridine or nicotinic receptor stimulation [8, 23], others suggest that, in the case of nicotinic stimulation, a major contribution of receptor- operated channels exists [1, 6, 10, 16--18]. Different species (bovine, feline, rodents) or preparations (perfused adrenal glands, isolated cells in suspensions or cultured) might explain these discrepancies; however, it is likely that various experimental de- signs (Na substitution by sucrose or choline, bicarbonate substitution by Tris(hyd- roxymethyl)aminomethane (Tris) or N-2-hydroxyethylplperazlne-N'-2-ethanesulfo- nic acid (HEPES) buffers, time of exposure of cells or glands to Na deprivation) might also contribute to the discrepancies [14]. It is not just a question of removing Correspondence A.G Garcta, Department of Pharmacology, Umversldad Aulonoma de Madrid, Facul- tad de Me&cma, ArzobJspo Morcillo, 4, 28029 Madrid, Spain_ 0304-3940/89/$ 03 50 © 1989 Elsevier Soentlfic Publishers Ireland Ltd.