Harvey Robert D
Department of Pharmacology, University of Nevada School of Medicine, Reno, NV 89557, USA.
Handb Exp Pharmacol. 2012(208):299-316. doi: 10.1007/978-3-642-23274-9_13.
Muscarinic receptor activation plays an essential role in parasympathetic regulation of cardiovascular function. The primary effect of parasympathetic stimulation is to decrease cardiac output by inhibiting heart rate. However, pharmacologically, muscarinic agonists are actually capable of producing both inhibitory and stimulatory effects on the heart as well as vasculature. This reflects the fact that muscarinic receptors are expressed throughout the cardiovascular system, even though they are not always involved in mediating parasympathetic responses. In the heart, in addition to regulating heart rate by altering the electrical activity of the sinoatrial node, activation of M₂ receptors can affect conduction of electrical impulses through the atrioventricular node. These same receptors can also regulate the electrical and mechanical activity of the atria and ventricles. In the vasculature, activation of M₃ and M₅ receptors in epithelial cells can cause vasorelaxation, while activation of M₁ or M₃ receptors in vascular smooth muscle cells can cause vasoconstriction in the absence of endothelium. This review focuses on our current understanding of the signaling mechanisms involved in mediating these responses.
毒蕈碱受体激活在心血管功能的副交感神经调节中起着至关重要的作用。副交感神经刺激的主要作用是通过抑制心率来降低心输出量。然而，从药理学角度来看，毒蕈碱激动剂实际上能够对心脏以及血管系统产生抑制和刺激两种作用。这反映出尽管毒蕈碱受体并非总是参与介导副交感神经反应，但它们在整个心血管系统中均有表达。在心脏中，除了通过改变窦房结的电活动来调节心率外，M₂受体的激活还可影响电冲动通过房室结的传导。这些相同的受体也能调节心房和心室的电活动和机械活动。在血管系统中，上皮细胞中M₃和M₅受体的激活可导致血管舒张，而在无内皮的情况下，血管平滑肌细胞中M₁或M₃受体的激活可导致血管收缩。本综述重点关注我们目前对介导这些反应所涉及的信号传导机制的理解。
