Ota M, Crofton J T, Toba K, Share L
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.
Proc Soc Exp Biol Med. 1992 Nov;201(2):208-14. doi: 10.3181/00379727-201-43500.
It is likely that central cholinergic pathways to the paraventricular and supraoptic nuclei participate in the control of vasopressin release. We have shown previously that this is due, in part, to activation of muscarinic, but not nicotinic, receptors in the paraventricular nucleus. There is, however, reason to believe that this cholinergic effect in the supraoptic nucleus may be the result of activation of nicotinic receptors. To test this possibility, we have studied in conscious unrestrained rats the effect of microinjection of muscarinic and nicotinic agonists into the supraoptic nucleus on vasopressin release, mean arterial blood pressure, and heart rate. Under ether anesthesia, a stainless steel guide cannula was placed in the supraoptic nucleus 5-7 days before the experiment, and femoral, arterial, and venous catheters were implanted 1 day before the experiment. Microinjection of nicotine into the supraoptic nucleus at doses of 1 and 10 micrograms resulted in transient increases in the plasma vasopressin concentration that were 7-fold and 11-fold greater, respectively, than control values at 3 min. There were also small transient increases in mean arterial blood pressure, but heart rate was unchanged. The microinjection of 2 and 20 ng of oxotremorine, a muscarinic agonist, into the supraoptic nucleus had no effect on the plasma vasopressin concentration, mean arterial blood pressure, or heart rate. These doses of oxotremorine were previously shown to have potent stimulatory effects on vasopressin release when microinjected into the paraventricular nucleus. These findings suggest that the central cholinergic stimulation of vasopressin release is due, in part, to activation of muscarinic receptors in the paraventricular nucleus and nicotinic receptors in the supraoptic nucleus.
中枢胆碱能通路至室旁核和视上核可能参与血管加压素释放的调控。我们之前已经表明，这部分是由于室旁核中M型胆碱能受体而非N型胆碱能受体的激活。然而，有理由相信视上核中的这种胆碱能效应可能是N型胆碱能受体激活的结果。为了验证这种可能性，我们在清醒不受束缚的大鼠中研究了向视上核微量注射M型和N型胆碱能激动剂对血管加压素释放、平均动脉血压和心率的影响。在乙醚麻醉下，于实验前5 - 7天将不锈钢引导套管置于视上核，于实验前1天植入股动脉和静脉导管。向视上核微量注射1微克和10微克剂量的尼古丁导致血浆血管加压素浓度短暂升高，在3分钟时分别比对照值高7倍和11倍。平均动脉血压也有小幅短暂升高，但心率未变。向视上核微量注射2纳克和20纳克毒扁豆碱（一种M型胆碱能激动剂）对血浆血管加压素浓度、平均动脉血压或心率均无影响。之前已表明，这些剂量的毒扁豆碱微量注射到室旁核时对血管加压素释放有强烈的刺激作用。这些发现表明，中枢胆碱能对血管加压素释放的刺激部分是由于室旁核中M型胆碱能受体和视上核中N型胆碱能受体的激活。
