Consideration of conduit and resistance vessels in regulation of blood flow.

In heart failure the maximal capacity for dilation, especially in skeletal muscle arteries, is reduced. This may be due to changes in sympathetic tone, in hormonal stimulation (both by circulating and intramurally released compounds like angiotensin II with additional presynaptic effects) or in endothelium mediated vasodilation. The loss of endothelium-mediated, flow-dependent dilation in large arteries may originate from endothelial impairment induced by, e.g., chronic hypoxia or hypercholesterolemia. Similar effects result from suppressed local dilator autacoid release brought about, e.g., by circulating atrial natriuretic factor in the presence of a fully functioning endothelium. Finally, attenuated augmentations in flow may be secondary to changes in muscular metabolism, and an increased alpha-adrenergic neurogenic constriction may be present. This may be further enhanced by a local, beta-receptor-mediated angiotensin II release. An impaired dilation at the level of resistance vessels may result from a combination of the mechanisms listed above.