Trimarchi G R, Germanò A, Campo G M, De Luca R, Caputi A P
Institute of Pharmacology, School of Medicine, University of Messina, Italy.
Life Sci. 1991;48(21):2097-107. doi: 10.1016/0024-3205(91)90167-a.
Activation of cholinergic neurons in specific brain regions evokes a hypernatriuretic response, which appears to be atropine-sensitive and, perhaps, independent from the renal innervation. However the role of cholinergic neurons in central control of renal function is not well understood. The purpose of this study was to further investigate whether brain acetylcholine stores are able to influence kaliuresis and natriuresis in conscious rats. Therefore, the renal response to cholinergic drugs was examined in Wistar rats which underwent to a 0.15 M NaCl solution (saline) load administered by gavage. Central injection of arecoline, a muscarinic agonist, produced a dose-dependent reduction in water diuresis and a highly significant increase in sodium excretion within two hours from the oral saline load. An intracerebroventricular (ICV) injection of methylatropine completely blocked both the antidiuretic and the natriuretic response induced by arecoline. Hemicholinium-3 (HC), centrally administered at a dose (34.8 nmol) known to be capable of inducing a maximal depletion of brain acetylcholine, elicited a time-dependent antidiuretic effect accompanied by a highly significant reduction in potassium and sodium urinary excretion. Therefore, we suggest that brain cholinergic neurons are involved in the regulation of the electrolyte balance.
特定脑区胆碱能神经元的激活会引发高钠利尿反应,该反应似乎对阿托品敏感,并且可能独立于肾神经支配。然而,胆碱能神经元在肾功能中枢控制中的作用尚未得到充分理解。本研究的目的是进一步探究脑内乙酰胆碱储备是否能够影响清醒大鼠的尿钾排泄和尿钠排泄。因此,在经口灌胃给予0.15 M氯化钠溶液(生理盐水)负荷的Wistar大鼠中,检测了对胆碱能药物的肾脏反应。中枢注射毒蕈碱激动剂槟榔碱,在口服生理盐水负荷后两小时内,产生了剂量依赖性的水利尿减少和钠排泄的高度显著增加。脑室内注射甲基阿托品完全阻断了槟榔碱诱导的抗利尿和利钠反应。以已知能够诱导脑内乙酰胆碱最大耗竭的剂量(34.8 nmol)中枢给予半胱氨酸-3(HC),引发了时间依赖性的抗利尿作用,并伴有钾和钠尿排泄的高度显著减少。因此,我们认为脑胆碱能神经元参与了电解质平衡的调节。