Intrinsic and Extrinsic Control of Circulation

Vascular tone — the tension exerted by vascular smooth muscle — determines the calibre of resistance vessels and therefore regional blood flow, arterial blood pressure, capillary recruitment, and central venous pressure. Vascular tone is controlled by intrinsic (local) and extrinsic (neural and hormonal) mechanisms.

The myogenic response is the first-line intrinsic mechanism. When arterial pressure rises, vessel wall stretch → L-type Ca2+ channels open → smooth muscle contracts → vasoconstriction restores normal flow (Bayliss myogenic response). This underlies flow autoregulation — maintaining constant blood flow despite pressure fluctuations. It is best developed in brain, myocardium, and kidney. When vessels constrict, increased shear stress stimulates endothelium to release NO → prevents excessive constriction. Decreased pressure → less stretch → vasodilation → restored perfusion.

Metabolic (active) hyperaemia occurs during increased tissue activity: ↑metabolic activity → ↓O2 (a vasoconstrictor) and ↑vasodilatory metabolites (CO2, H+, lactic acid, adenosine) → arteriolar vasodilation → increased blood flow proportional to demand. Reactive hyperaemia occurs after complete vessel occlusion: distal ischaemia → metabolite accumulation → vasodilation → massive flow surge when obstruction is relieved. It underlies symptoms in myocardial infarction and peripheral artery disease.

Endothelial paracrine control: nitric oxide (NO) is produced mainly in response to shear stress (60-80%) and to a lesser extent by insulin and oestrogen. NO has a half-life of ~6 seconds and causes smooth muscle relaxation (vasodilation). NO-mimicking drugs — glyceryl trinitrate, isosorbide dinitrate, sodium nitroprusside — treat angina by reducing venous preload and systolic afterload.

Extrinsic control is dominated by sympathetic vasoconstrictor nerves. These innervate most arterioles and veins, are tonically active (~1 impulse/s), and release noradrenaline and ATP at varicosities. Noradrenaline binds α-adrenoceptors → vasoconstriction. A fall in activity (or α-blockers) causes vasodilation. Vasodilator parasympathetic fibres release ACh → M3 receptors on endothelium → eNOS → NO → vasodilation. Hormonal factors include adrenaline (α1/β2-mediated variable effects), angiotensin II (vasoconstriction in hypovolaemia/failure), vasopressin/ADH (vasoconstriction in hypovolaemia), and atrial natriuretic peptide (moderate vasodilation and diuresis).