What Is an Acetylcholine Deficiency?

Acetylcholine is a neurotransmitter. It is rapidly destroyed in tissues by cholinesterase. Acetylcholine can specifically act on various choline receptors, but it has a wide range of effects and is not highly selective. It is not clinically used as medicine, and it is generally only used for experimental medicine. In nerve cells, acetylcholine is synthesized by choline and acetyl-CoA under the catalysis of choline acetyltransferase (choline acetylase). Mainstream research suggests that an increase in the substance's content in the body is significantly associated with improved symptoms of Alzheimer's disease (Alzheimer's disease).

Acetylcholine cardiovascular system

Cardiovascular system ACh has the following effects on the cardiovascular system:

Synthesis and role of acetylcholine in synapses

(1) Vasodilation effect: Intravenous injection of a small dose of this product can cause a temporary decrease in blood pressure due to systemic vasodilation, and is accompanied by an accelerated reflex heart rate. ACh can cause many blood vessels to dilate. Such as the lungs and coronary vessels. Its vasodilator effect is mainly due to the activation of vascular endothelial cells M and choline receptor subtypes, leading to the release of endothelial-dependent relaxing factor (EDRF), which is nitric oxide (No), thereby causing adjacent smooth muscle cells to relax. Caused by baroreceptor or chemoreceptor reflexes. If the vascular endothelium is damaged, the above-mentioned effects of ACh will no longer exist, instead it will cause vasoconstriction. In addition, ACh inhibits the release of NA from noradrenergic nerve endings by stimulating the presynaptic M1 receptor in sympathetic nerve endings, which is also related to the vasodilating effect of ACh.

(2) Slow heart rate: also known as negative frequency effect. ACh can delay the depolarization of the sinoatrial node automatically, delay the repolarization current, increase the repolarization current, extend the time for the action potential to reach the threshold, and cause the heart rate to slow.

(3) Slow atrioventricular node and Purkinje fiber conduction: negative conduction effect. ACh prolongs the refractory period of the atrioventricular node and Purkinje fibers, slowing their conduction. When cardiac glycosides are used to increase vagal tone or systemic administration of high-dose choline receptor agonists, complete cardiac blockade is often associated with a significant suppression of atrioventricular node conduction.

(4) Attenuation of myocardial contractility: negative muscle effect. It is generally believed that cholinergic nerves are mainly distributed in the sinoatrial node, atrioventricular node, Purkinje fibers, and the atrium, and the ventricle is less innervated with cholinergic nerves, so ACh has a greater inhibitory effect on atrial contraction than the ventricle. However, because the vagus nerve terminal is closely adjacent to the sympathetic nerve terminal, the ACh released by the vagal nerve terminal can stimulate the presynaptic M choline receptors of the sympathetic nerve terminal, and feedbackally inhibit the norepinephrine release of the sympathetic nerve terminal. Reduces ventricular contractility.

(5) Shorten 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 duration (ie, vagus nerve effect).

Acetylcholine gastrointestinal tract

ACh can obviously stimulate the smooth muscle of the gastrointestinal tract, increase its contraction amplitude, tension, and peristalsis, and can promote gastric and intestinal secretions, causing symptoms such as nausea, belching, vomiting, abdominal pain and defecation.

Acetylcholine urinary tract

ACh can increase urinary smooth muscle peristalsis, bladder detrusor contraction, increase the maximum voluntary emptying pressure of the bladder, reduce the bladder volume, and at the same time relax the bladder triangle and external sphincter, leading to bladder emptying.

Acetylcholine other

(1) Glands: ACh can increase the secretion of lacrimal glands, trachea and bronchial glands, salivary glands, digestive tract glands, and sweat glands.

(2) Eyes: When ACh is dripped locally, it can cause pupil contraction and adjust to myopia.

(3) Ganglion and skeletal muscle: ACh acts on autonomic ganglion NN choline receptors and NM choline receptors of skeletal muscle neuromuscular junctions, causing sympathetic, parasympathetic ganglion excitement and skeletal muscle contraction. In addition, because adrenal medulla is dominated by post-sympathetic ganglia fibers, NN choline receptor agonism can cause adrenaline release.

(4) Central: Because ACh is not easy to enter the central nervous system, although there are choline receptors in the central nervous system, peripheral administration rarely produces central effects.

(5) Bronchus: ACh can cause bronchoconstriction.

(6) ACh can also excite carotid body and aortic body chemical receptors. ^[3]