Sodium-dependent and sodium-independent nicotine-evoked catecholamine release from cat adrenals.
Cat adrenal glands were stimulated with nicotine under Na-free conditions; subsequently, Na was gradually introduced as a continuously increasing gradient from 0 to 134 mM. With this experimental approach two catecholamine secretory peak responses were obtained: one was Na-independent 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 dihydropiridine Ca channel blocker. The results suggest that Na, although not essential to evoke some degree of secretion, plays, however, a prominent role in amplifying the nicotine-secretory response by causing cell depolarization and opening of voltage-dependent Ca channels.
Abajo
F J
FJ
Department of Pharmacology, Universidad Autonoma de Madrid, Facultad de Medicina, Spain.
Castro
M A
MA
Lopo
C R
CR
Garijo
B
B
Sanchez-Garcia
P
P
Garcia
A G
AG
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002395:Catecholamines / Q000378:metabolism*; D002415:Cats; D008564:Membrane Potentials / Q000187:drug effects; D009538:Nicotine / Q000494:pharmacology*; D012964:Sodium / Q000494:pharmacology*; D013997:Time Factors
D002395:Catecholamines; D009538:Nicotine; D012964:Sodium