The main role of acetylcholine in the cardiovascular system

The main role of acetylcholine in the cardiovascular system:

The main role of acetylcholine in the cardiovascular system

(1) Vasodilatation: intravenous injection of small doses of this product may cause a temporary drop in blood pressure due to systemic vasodilation, accompanied by a reflex heart rate. ACh can cause many vasodilatations. Such as the lungs and coronary vessels. Its vasodilator effect is mainly due to inflammatory endothelial cells M, choline receptor subtype, leading to the release of endothelium-dependent relaxation factor (EDRF), nitric oxide (No), which causes relaxation of adjacent smooth muscle cells, possibly through Caused by baroreceptors or chemoreceptors. If the vascular endothelium is damaged, the above effects of ACh will no longer exist, which in turn may cause vasoconstriction. In addition, ACh inhibits the release of NA from noradrenergic nerve endings by activating the presynaptic M1 receptor in sympathetic nerve terminals and is also associated with ACh vasodilation.

(2) Slow heart rate: also known as negative frequency effect. ACh can delay the auto-depolarization of the sinus node diastolic phase, increase the repolarization current, and prolong the action potential to reach the threshold, resulting in slow heart rate.



(3) Slowing atrioventricular node and Pukenye fiber conduction: it is negative conduction. ACh can prolong the refractory period of the atrioventricular node and Βurkinje fibers, causing their conduction to slow down. Complete heart blockade that occurs when cardiac glycoside is used to increase vagal tone or systemic administration of high-dose choline receptor agonists is often associated with significant inhibition of atrioventricular node conduction.

(4) Weakening myocardial contractility: that is, negative muscle strength. It is generally believed that cholinergic nerves are mainly distributed in the sinus node, atrioventricular node, Pukenye fiber and atrium, while the ventricle is less cholinergic innervation, so ACh inhibits atrial contraction more than the ventricle. However, because the vagus nerve endings are closely adjacent to the sympathetic nerve endings, ACh released from the vagus nerve terminals can stimulate the presynaptic M choline receptors in the sympathetic nerve terminals, and feedback-represses the release of norepinephrine from the sympathetic nerve terminals. Reduces ventricular contractility.

(5) Shortening the atrial refractory period: ACh does not affect the conduction velocity of the atrial muscle, but can shorten the atrial refractory period and the action potential time course (that is, the vagus nerve action).