Systemic vascular resistance and coronary vessel tone
THE CONTEXT
Resistance vessels regulate systemic blood flow through changes in radius and smooth muscle tone. Coronary vessels also use autonomic and homeostatic mechanisms to regulate flow.
Determinants of vascular resistance
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Progressive arterial stiffening occurs with ageing and kidney disease.
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Vascular smooth muscle has a progressively greater role farther along the arterial tree, reaching the resistance arterioles.
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Resistance vessels, with diameters of 50–200 μm, make the greatest contribution to systemic vascular resistance, although all vessels contribute.
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Resistance is inversely proportional to the fourth power of radius according to Poiseuille’s law, so small changes in radius markedly influence blood flow.
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Resistance rises with blood viscosity, which is mainly influenced by the haematocrit.
Regulation of resistance vessel tone
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Humoral, neuronal and mechanical factors tightly regulate resistance vessel tone.
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Neurogenic constriction operates through α-adrenoceptors on vascular smooth muscle; dilatation operates through muscarinic and β2-adrenoceptors.
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Noradrenaline, also called norepinephrine, angiotensin II and endothelin-1 are vasoconstrictors.
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Adenosine, bradykinin, prostaglandins and nitric oxide are vasodilators.
Coronary regulation and stenosis
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Coronary vessels receive sympathetic and parasympathetic innervation.
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Coronary α-adrenoceptor stimulation causes vasoconstriction, whereas β2-adrenoceptor stimulation causes vasodilatation. The predominant effect of sympathetic stimulation in coronary arteries is vasodilatation.
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Parasympathetic stimulation produces modest dilatation of healthy coronary arteries.
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Homeostatic regulation of vessel tone preserves coronary flow, even during exercise, until stenosis reduces vessel cross-sectional area by at least 70%.