Abstract
Nitric oxide is a vital signalling molecule that controls blood flow and pressure. Unexpectedly, a redox switch in the protein haemoglobin α within endothelial cells regulates this molecule's diffusion in blood vessels. See Letter p.473 This manuscript provides evidence for a new model of the regulation of nitric oxide signalling in myoendothelial gap junctions. The oxidation state of endothelial haemoglobin α, controlled by cytochrome b5 reductase 3, regulates nitric oxide bioavailability and diffusion towards its vascular smooth muscle targets by promoting either the formation of vasodilator S-nitrosothiols or the scavenging of nitric oxide. This endothelial regulation of nitric oxide modulates the effects of agents involved in the control of vascular tone, such as α-adrenergic agonists or substances that evoke endothelium-dependent relaxations.
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