What is the function of acetylcholine

Acetylcholine is a cholestatic neurotransmitter and is actually widely used clinically because it can dilate blood vessels. It can also slow down the heart rate and slow down the conduction of the atrioventricular node and Purkinje fibers. We should pay attention to these effects.

(1) Vasodilator effect

Intravenous injection of small doses of this product can cause a transient drop in blood pressure due to systemic vasodilation, accompanied by a reflex increase in heart rate. ACh can cause many blood vessels to dilate. Such as the lungs and coronary vessels. Its vasodilatory effect is mainly due to the stimulation of endothelial cell M, choline receptor subtype, leading to the release of endothelium-dependent relaxing factor (EDRF), also known as nitric oxide (nitric oxide).

The release of NO (nitric oxide, or NO) causes the relaxation of adjacent smooth muscle cells, and may also be caused by pressure receptors or chemoreceptor reflexes. If the vascular endothelium is damaged, the above-mentioned effects of ACh will no longer exist, and instead it may cause vasoconstriction. In addition, ACh stimulates the presynaptic M1 receptors of sympathetic nerve endings and inhibits the release of NA from noradrenergic nerve endings, which is also related to the vasodilation effect of ACh.

Intravenous injection of a small dose of this drug can cause a temporary drop in blood pressure due to systemic vasodilation.

(2) Slow down your heart rate

Also known as negative frequency action, ACh can delay the automatic depolarization of the sinoatrial node during diastole, increase the repolarization current, prolong the time it takes for the action potential to reach the threshold, and cause a slower heart rate.

(3) Slow down the conduction of atrioventricular node and Purkinje fibers

The negative conduction effect of acetylcholine can prolong the refractory period of the atrioventricular node and Purkinje fibers, β-urkinje fibers, and slow down conduction. Complete heart block is often related to depression of atrioventricular nodal conduction when cardiac glycosides are used to increase vagal tone or when high doses of systemically administered acetylcholine receptor agonists are used.

(4) Weakened myocardial contractility

That is, it has a negative inotropic effect. It is generally believed that the cholesterin nerves are mainly distributed in the sinoatrial node, atrioventricular node, Purkinje fibers and atria, while the ventricles are less innervated by cholesterin nerves. Therefore, the inhibitory effect of ACh on atrial contraction is greater than that on ventricle. However, since the vagus nerve endings are closely adjacent to the sympathetic nerve endings, the ACh released by the vagus nerve endings can excite the presynaptic M choline receptors of the sympathetic nerve endings, feedback inhibiting the release of norepinephrine from the sympathetic nerve endings. Weakens the force of ventricular contraction.