What is the role of acetylcholine in vasodilation

Blood vessels are affected by diseases, environment, age, etc., which can cause many symptoms, and serious diseases are prone to occur that harm the blood vessels. For example, if the blood vessels are narrow or small, the patient can undergo vasodilation treatment. There are many commonly used treatment methods, which need to be analyzed and judged according to the condition of the blood vessels. Acetylcholine is also widely used to dilate blood vessels, and patients can use this treatment to regulate their blood vessels. So what is the role of acetylcholine in vasodilation?

Acetylcholine, with the molecular formula CH3COOCH2CH2N+(CH3)3, is a neurotransmitter that can specifically act on various types of choline receptors, but its effects are broad and its selectivity is not high. It is rapidly destroyed in tissues by cholesterase, which has a wide range of effects and is not very selective. It is not used as medicine in clinical practice and is generally only used as an experimental drug. In nerve cells, acetylcholine is synthesized from choline and acetyl-CoA under the catalysis of choline acetyltransferase (choline acetyltransferase). Mainstream research believes that the content of this substance in the body is significantly correlated with the improvement of symptoms of Alzheimer's disease (senile dementia).

(1) Vasodilator effect: Intravenous injection of a small dose of this drug 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 vasodilation effect is mainly due to the stimulation of vascular endothelial cell M, choline receptor subtype, leading to the release of endothelium-dependent relaxing factor (EDRF), namely nitric oxide (No), thereby causing relaxation of adjacent smooth muscle cells. It 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.

(2) Slowing down the heart rate: also known as negative frequency effect. 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 the atrioventricular node and Purkinje fibers: this is the negative conduction effect. ACh can prolong the refractory period of the atrioventricular node and Purkinje fibers, slowing down their conduction. Complete heart block that occurs when vagal tone is increased with cardiac glycosides or when high doses of cholecystokinin receptor agonists are administered systemically is often associated with a marked inhibition of atrioventricular nodal conduction.

(4) Weakens myocardial contractility: this is known as negative inotropic effect. It is generally believed that cholestatic nerves are mainly distributed in the sinoatrial node, atrioventricular node, Purkinje fibers and atria, while the ventricles are less innervated by cholestatic nerves. Therefore, the inhibitory effect of ACh on atrial contraction is greater than that on ventricular contraction. 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.

(5) Shorten the atrial refractory period: ACh does not affect the conduction velocity of the atrial muscle, but it can shorten the atrial refractory period and action potential duration (i.e., the vagal effect).

First, it causes sympathetic nerve excitement in the body, causing transient vasospasm and increased blood pressure; but soon the parasympathetic nerves are excited and vasodilation occurs, which causes a drop in blood pressure, resulting in insufficient blood supply to the cerebral cortex and a loss of regulatory ability on the lower centers, causing autonomic nervous system dysfunction. Then there will be pale complexion, sweating, dizziness, cold limbs, nausea and vomiting, rapid heartbeat, and a drop in blood pressure. Some people will experience incontinence and even faint on the ground. In the absence of a clear cause, do not use drugs indiscriminately on your own, as this will easily delay the disease. Please seek treatment in a regular hospital to ensure effective treatment.

What is the role of acetylcholine in vasodilation? Its role is enormous. Many people do not understand the disease when they hear such a professional term. Clinical diseases are very complex and there are many types. It is difficult for patients to master the relevant knowledge of the disease. However, when you find that you are feeling unwell and you cannot judge for yourself, you can do a comprehensive physical examination or a targeted examination to determine the severity of the disease and provide reasonable treatment.