If blood vessels mostly aren’t supplied by parasympathetic nerves, how effects through M3-ACh receptors are mediated?
Although blood vessels are not primarily innervated by parasympathetic nerves, they are still influenced by the parasympathetic nervous system through a secondary mechanism. The effects on blood vessels mediated by M3-ACh receptors are primarily indirect, involving the release of neurotransmitters and hormones.
When the parasympathetic nervous system is activated, acetylcholine (ACh) is released from parasympathetic nerve terminals. ACh then binds to M3 muscarinic receptors located on endothelial cells lining the blood vessels. This binding results in the release of nitric oxide (NO) from the endothelial cells.
NO is a potent vasodilator, meaning it relaxes and widens blood vessels. Once released, NO diffuses into the smooth muscle cells of the blood vessel walls, causing them to relax. This relaxation leads to vasodilation and increased blood flow in the affected vessels.
In addition to NO release, ACh binding to M3 receptors on endothelial cells can also stimulate the release of other vasodilators like prostacyclin and endothelium-derived hyperpolarizing factor (EDHF). These substances further contribute to the relaxation and dilation of blood vessels.
It’s important to note that the parasympathetic nervous system’s influence on blood vessels is secondary to the primary control exerted by the sympathetic nervous system. Sympathetic nerves, also known as adrenergic nerves, innervate blood vessels and release norepinephrine onto alpha-adrenergic receptors. This binding causes vasoconstriction, which decreases blood flow.
Overall, although blood vessels are not directly supplied by parasympathetic nerves, the effects mediated through M3-ACh receptors involve the release of vasodilators like nitric oxide, prostacyclin, and EDHF from endothelial cells. These vasodilators counterbalance the vasoconstrictive effect of sympathetic nerve activity, maintaining proper blood flow regulation.
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