Vascular smooth muscle in the tunica media of arteries and arterioles is the primary effector of blood pressure regulation and local blood flow distribution. Its tone is governed by a balance of vasoconstrictor (sympathetic, endothelin, angiotensin II) and vasodilator (NO, prostacyclin, beta-2) signals. Dysfunction or remodelling of vascular smooth muscle contributes to hypertension, atherosclerosis, and vasospasm.
| Origin | Tunica media of arteries and arterioles throughout the body: multiple smooth muscle cell layers in large arteries (aorta 40-70 layers); single smooth muscle cell layer in arterioles; capillaries and venules lack smooth muscle; veins have a thin muscular coat |
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| Insertion | Continuous circumferential arrangement in the vessel wall; no discrete origin or insertion; smooth muscle cells connect to the elastic laminae and to each other via gap junctions |
| Nerve Supply | Sympathetic adrenergic fibres (alpha-1 receptors — vasoconstriction; beta-2 — vasodilation in skeletal muscle); Parasympathetic acetylcholine (endothelium-dependent vasodilation via NO); Local factors (endothelin, angiotensin II — vasoconstriction; prostacyclin, NO — vasodilation) |
| Blood Supply | Self-supplied via the vasa vasorum (vessels of vessels) in large arteries; directly from the lumen by diffusion in small arteries |
| Actions | Contraction narrows the vascular lumen (vasoconstriction), increasing vascular resistance and blood pressure; relaxation widens the lumen (vasodilation), decreasing resistance; tone is the primary determinant of peripheral vascular resistance and blood pressure regulation; arterial smooth muscle sustains pulsatile flow by elastic recoil |
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Hypertension involves vascular smooth muscle remodelling with medial hypertrophy, increasing peripheral vascular resistance. Antihypertensive drugs target vascular smooth muscle via multiple pathways: calcium channel blockers (amlodipine — prevent calcium-mediated contraction), ACE inhibitors and ARBs (reduce angiotensin II vasoconstrictive tone), alpha-1 blockers (doxazosin — block sympathetic vasoconstriction). Raynaud's phenomenon involves episodic vascular smooth muscle vasospasm in peripheral arteries producing digital ischaemia from cold and emotional stress. Coronary artery vasospasm (Prinzmetal's angina) produces angina at rest from focal coronary smooth muscle spasm.
Focal coronary artery smooth muscle spasm produces transient transmural ischaemia at rest with ST elevation on ECG that resolves spontaneously or with nitrates; calcium channel blockers (verapamil, diltiazem) prevent smooth muscle vasoconstriction and are the primary prophylactic therapy for Prinzmetal's angina.
