Acetylcholine (ACh)

Human brain tissue has a large amount of acetylcholine, but the content of acetylcholine decreases with age. Normal elderly people are 30% lower than in youth, while those with dementia are more severe, reaching 70% to 80%. American doctor Wu Weman observed that the acetylcholine in the brain tissue of the elderly was reduced, and the elderly were given choline-rich foods, and it was found to have obvious effects of preventing memory loss. Scientists in countries such as the United Kingdom and Canada have also conducted research, agreeing that as long as the supply of adequate choline is controlled, the memory loss of the elderly in the 60s can be avoided. Therefore, maintaining and improving the content of acetylcholine in the brain is the fundamental way to solve the memory loss. In nature, acetylcholine is mostly present in the form of choline in eggs, fish, meat, soybeans, etc. These choline must be biochemically reacted in the human body to synthesize physiologically active acetylcholine. In addition, regular consumption of royal jelly can increase the content of acetylcholine in the brain, thereby promoting the activation of cranial nerve conduction function, improving the speed of information transmission, enhancing brain memory, comprehensively improving brain function, and delaying ageing.

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

Synthesis and role of acetylcholine in synapses

(1) vasodilatation: intravenous injection of small doses of this product can cause a brief 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 of 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 suppresses 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 duration (that is, the vagus nerve).

Gastrointestinal

ACh can obviously excite the smooth muscle of the gastrointestinal tract, increase its contraction amplitude, tension and peristalsis, and promote gastric and intestinal secretion, causing symptoms such as nausea, belching, vomiting, abdominal pain and defecation.
Urinary tract
ACh can increase the smooth muscle peristalsis of the urinary tract, contraction of the bladder detrusor, increase the maximum voluntary emptying pressure of the bladder, reduce the bladder volume, and relax the bladder triangle and the external sphincter, leading to bladder emptying.

other

(1) Gland: ACh can increase the secretion of lacrimal gland, trachea and bronchial glands, salivary glands, digestive tract glands and sweat glands.
(2) Eye: When ACh is partially instilled, it can cause the pupil to contract and adjust to myopia.
(3) ganglion and skeletal muscle: ACh acts on the NM choline receptors of the autonomic ganglia NN choline receptor and skeletal muscle neuromuscular junction, causing sympathetic, parasympathetic ganglion excitation and skeletal muscle contraction. In addition, because the adrenal medulla is innervated by sympathetic ganglion fibers, NN choline receptor agonism can cause adrenaline release.
(4) Central: Since ACh is not easy to enter the human center, although the central nervous system has choline receptors, peripheral administration rarely produces a central role.
(5) Bronchial: ACh can cause bronchoconstriction.
(6) ACh can also excite the carotid body and aortic body chemical receptors.