Aim:To study the effect of arecoline,an alkaloid isolated from Areca catechu,onthe secretion of catecholamines (CA) evoked by cholinergic agonists and themembrane depolarizer from isolated perfused rat adrenal gland.Methods:Adrenalglands were isolated from male Sprague-Dawley rats.The adrenal glands wereperfused with Krebs bicarbonate solution by means of a peristaltic pump.The CAcontent of the perfusate was measured directly using the fluorometric method.Results:Arecoline (0.1-1.0 mmol/L) perfused into an adrenal vein for 60 min pro-duced dose-and time-dependent inhibition in CA secretory responses evoked byacetylcholine (ACh) (5.32 mmol/L),1.1-dimethyl-4-phenyl piperazinium iodide(DMPP) (100μmol/L for 2 min) and 3-(m-choloro-phenyl-carbamoyl-oxy)-2-butynyltrimethyl ammonium chloride (McN-A-343)(100μmol/L for 2 min).However,lowerdoses of arecoline did not affect CA secretion of high K~+(56 mmol/L);higherdoses greatly reduced CA secretion of high K~+.Arecoline also failed to affectbasal catecholamine output.Furthermore,in adrenal glands loaded with arecoline(0.3 mmol/L),CA secretory response evoked by Bay-K-8644 (10μmol/L),an activa-tor of L-type Ca~(2+) channels,was markedly inhibited,whereas CA secretion bycyclopiazonic acid(10μmol/L),an inhibitor of cytoplasmic Ca~(2+)-ATPase,was notaffected.Nicotine (30μmol/L),which was perfused into the adrenal gland for 60min,however,initially enhanced ACh-evoked CA secretory responses.As timeelapsed,these responses became more inhibited,whereas the initially enhancedhigh K~+-evoked CA release diminished.CA secretion evoked by DMPP and McN-A-343 was significantly depressed in the presence of nicotine.Conclusion:Arecoline dose-dependently inhibits CA secretion from isolated perfused rat ad-renal gland evoked by activation of cholinergic receptors.At lower doses arecolinedoes not inhibit CA secretion through membrane depolarization,but at largerdoses it does.This inhibitory effect of arecoline may be mediated by blocking thecalcium influx into the rat adrenal medullary chromaffin cells without the inhibitionof Ca~(2+) release from the cytoplasmic calcium store.There seems to be a differencein the mode of action of nicotine and arecoline in rat adrenomedullary CA secretion. Aim: To study the effect of arecoline, an alkaloid isolated from Areca catechu, on the secretion of catecholamines (CA) evoked by cholinergic agonists and themembrane depolarizer from isolated perfused rat adrenal gland. Methods: Adrenalglands were isolated from male Sprague-Dawley rats. The CAcontent of the perfusate was measured directly using the fluorometric method. Results: Arecoline (0.1-1.0 mmol / L) perfused into an adrenal vein for 60 min pro-duced dose -and time-dependent inhibition in CA secretory responses evoked by acetylcholine (ACh) (5.32 mmol / L), 1.1-dimethyl- 4-phenyl piperazinium iodide (100 μmol / L for 2 min) and 3- However, lower doses of arecoline did not affect CA secretion of high K ~ + (56 mmol / L); phenyl-carbamoyl-oxy) -2-butynyltrimethyl ammonium chloride (McN- higherdoses greatly reduced CA secretion of high K ~ + .Arecoline also failed to affectba sal catecholamine output.Furthermore, in adrenal glands loaded with arecoline (0.3 mmol / L), CA secretory response evoked by Bay-K-8644 (10 μmol / L), an activa-tor of L-type Ca 2+ channels , was markedly inhibited, while CA secretion by cyclopiazonic acid (10 μmol / L), an inhibitor of cytoplasmic Ca ~ (2 +) - ATPase, was not affected by Nicotine (30 μmol / L), which was perfused into the adrenal gland for 60 min, , initially enhanced ACh-evoked CA secretory responses. As timeelapsed, these responses became more inhibited, but the initially enhanced high K ~ + -evoked CA release diminished. CA secretion evoked by DMPP and McN-A-343 was significantly depressed in the presence of nicotine.Conclusion: Arecoline dose-dependently inhibits CA secretion from isolated perfused rat ad-renal gland evoked by activation of cholinergic receptors. At lower doses arecolinedoes not inhibit CA secretion through membrane depolarization, but at larger waves it does. so inhibitory effect of arecoline may be mediated by blocking th ecalcium influx into the rat adrenal medullary chromaffin cells without the inhibition of Ca ~ (2+) release from the cytoplasmic calcium store. where seems to be a difference in the mode of action of nicotine and arecoline in rat adrenomedullary CA secretion.