Sorimachi M, Nishimura S
Jpn J Physiol. 1982;32(4):541-51. doi: 10.2170/jjphysiol.32.541.
Cat adrenal glands were retrogradely perfused in vitro with modified Locke's medium and the mechanism of catecholamine (CA) secretion induced by choline was investigated. Choline-induced secretion of CA was accompanied by release of dopamine-beta-hydroxylase, but not by that of phenylethanolamine-N-methyl transferase, indicating that an exocytotic mechanism is involved in the secretion. Choline failed to induce the secretion of CA when Ca was absent from the perfusion solution. On the other hand, secretion increased when the concentration of Ca2+ in the perfusion medium was raised to 10 mM. Stimulation of secretion by choline was observed from a concentration of 1 mM, and half-maximal secretion occurred at about 10 mM. The stimulatory action was weaker than that of acetylcholine(ACh); the effect of 100 mM choline was approximately equal to that of 0.02 mM ACh. Secretion induced by a low concentration of choline was abolished by a nicotinic blocker, hexamethonium, while the response to choline at a concentration higher than 130 mM was only partially inhibited by cholinergic antagonists. The effects of choline and a low concentration of ACh were additive. On the other hand, 100 mM choline inhibited the response to a supramaximal concentration of ACh(0.5 mM), suggesting that ACh and choline stimulate the same nicotinic receptor. It is concluded that choline acts partially as a nicotinic agonist and that a concentration higher than 130 mM causes secretion by a mechanism additional to nicotinic receptor activation.
采用改良洛克氏液对猫的肾上腺进行体外逆行灌注，研究胆碱诱导儿茶酚胺（CA）分泌的机制。胆碱诱导的CA分泌伴随着多巴胺-β-羟化酶的释放，但苯乙醇胺-N-甲基转移酶未释放，表明分泌过程涉及胞吐机制。当灌注液中无钙时，胆碱未能诱导CA分泌。另一方面，当灌注培养基中Ca2+浓度提高到10 mM时，分泌增加。从1 mM的浓度开始观察到胆碱对分泌的刺激作用，约10 mM时出现半数最大分泌。其刺激作用比乙酰胆碱（ACh）弱；100 mM胆碱的作用约等于0.02 mM ACh的作用。低浓度胆碱诱导的分泌被烟碱阻断剂六甲铵消除，而高于130 mM浓度的胆碱引起的反应仅被胆碱能拮抗剂部分抑制。胆碱和低浓度ACh的作用是相加的。另一方面，100 mM胆碱抑制对超最大浓度ACh（0.5 mM）的反应，表明ACh和胆碱刺激相同的烟碱受体。结论是胆碱部分作为烟碱激动剂起作用，高于130 mM的浓度通过烟碱受体激活以外的机制引起分泌。
