Arecoline inhibits catecholamine release from perfused rat adrenal gland

Dong-yoon LIM; Il-sik KIM

摘要

Aim: To study the effect of arecoline, an alkaloid isolated from Areca catechu, on the secretion of catecholamines (CA) evoked by cholinergic agonists and the membrane depolarizer from isolated perfused rat adrenal gland. Methods: Adrenal glands were isolated from male Sprague-Dawley rats. The adrenal glands were perfused with Krebs bicarbonate solution by means of a peristaltic pump. The CA content 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 produced dose- and time-dependent inhibition in CA secretory responses evoked by acetylcholine (ACh) (5.32 mmol/L), 1.1-dimethyl-4-phenyl piperazinium iodide (DMPP) (100 μmol/L for 2 min) and 3-(m-choloro-phenyl-carbamoyl-oxy)-2-butynyl trimethyl ammonium chloride (McN-A-343) (100 μmol/L for 2 min). However, lower doses of arecoline did not affect CA secretion of high K+ (56 mmol/L); higher doses greatly reduced CA secretion of high K+. Arecoline also failed to affect basal 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 activator of L-type Ca2+ channels, was markedly inhibited, whereas CA secretion by cyclopiazonic acid (10 μmol/L), an inhibitor of cytoplasmic Ca2+-ATPase, was not affected. Nicotine (30 μmol/L), which was peffused into the adrenal gland for 60min, however, initially enhanced ACh-evoked CA secretory responses. As time elapsed, these responses became more inhibited, whereas the initially enhanced high K+-evoked CA release diminished. CA secretion evoked by DMPP and McNA-343 was significantly depressed in the presence of nicotine. Conclusion:Arecoline dose-dependently inhibits CA secretion from isolated perfused rat adrenal gland evoked by activation of cholinergic receptors. At lower doses arecoline does not inhibit CA secretion through membrane depolarization, but at larger doses it does. This inhibitory effect of arecoline may be mediated by blocking the calcium influx into the rat adrenal medullary chromaffin cells without the inhibition of Ca2+ release from the cytoplasmic calcium store. There seems to be a difference in the mode of action of nicotine and arecoline in rat adrenomedullary CA secretion.

机译：目的：研究氨基啉的作用，从槟榔分离的生物碱，在胆碱能激动剂和膜去偏振器中引起的儿茶胺（CA）分泌来自分离的灌注大鼠肾上腺腺瘤的分泌。方法：从雄性Sprague-Dawley大鼠中分离肾上腺腺体。通过蠕动泵用Krebs碳酸氢盐溶液灌注肾上腺。使用荧光法直接测量灌注液的Ca含量。结果：氨基啉（0.1-1.0mmol / L）灌注到肾上腺静脉中的60分钟产生的Ca分泌反应产生的剂量和时间抑制（ACH ）（5.32mmol / L），1.1-二甲基-4-苯基哌嗪碘化钛（DMPP）（100μmol/ L持续2分钟）和3-（M-Choloro-苯基 - 氨基酰基-Noy）-2-丁炔基三甲基氯化铵（MCN-A-343）（100μmol/ L 2分钟）。然而，较低剂量的杏仁不影响高k +（56mmol / L）的Ca分泌;较高剂量大大降低了高K +的Ca分泌。杏仁也未能影响基础儿茶酚胺输出。此外，在装载areColine（0.3mmol / L）的肾上腺中，通过环-K-8644（10μmol/ L）引起的Ca分泌响应，L型Ca2 +通道的活化剂，抑制，而Cyclopiazonic的Ca分泌酸（10μmol/ L），细胞质Ca2 + -Atpase的抑制剂不受影响。然而，尼古丁（30μmol/ L）被培养到肾上腺60min中，最初增强了Ach-Excoked Ca分泌反应。随着时间的推移，这些反应变得更加抑制，而最初增强的高K +次升高的CA释放减少了。在尼古丁存在下，DMPP和MCNA-343引起的Ca分泌显着抑制。结论：氨基啉剂量依赖性抑制来自胆碱能受体的激活诱捕的分离的灌注大鼠肾上腺腺癌的Ca分泌。在较低剂量的葡萄球中，不抑制Ca分泌通过膜去极化，但它的剂量较大。可以通过将钙流入流入大鼠肾上腺髓质斑铬细胞中的钙流入而不抑制来自细胞质钙储存的CA2 +释放来介导的这种抑制作用。在大鼠肾上腺素髓质Ca分泌中尼古丁和葡萄啉的作用方式似乎存在差异。

Arecoline inhibits catecholamine release from perfused rat adrenal gland

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