Vascular oxygen sensors

Roles for NAD(P)H Oxidases as Vascular Oxygen Sensors and Their Influence on Oxidant-Regulated Signaling Mechanisms... 

Hypoxia also causes the release of adenosine from cardiac myocytes. Adenosine in a potent dilator of coronary arteries. It has been shown that adenosine activates K xp currents in single coronary artery smooth muscle cells (Dart and Standen, 1993, 1994). Activation of the K xp channel is also involved in the hypoxic vasodilation in the cerebral, renal (Loutzen-hiser and Parker, 1994), skeletal muscle, and cremaster muscle and cheek pouch circulations (see Nelson and Quayle, 1995). Activation of K xp channels in these vascular beds may be a direct consequence of hypoxia on a smooth muscle oxygen sensor, an effect of hypoxia on smooth muscle cell metabolism, or through the release of vasodilator metabolites like adenosine from surrounding tissue, similar to hypoxic coronary vasodilation. 

The adaptation of tissue blood flow to local metabolic requirements is a dramatic example of the control of smooth muscle contraction by metabolic factors. The exact mechanisms involved are still not known with certainty, and in particular it is not clear how much is due to a direct response of the vascular smooth muscle to its chemical environment and how much is due to "vasodilator metabolites" released from the tissue parenchyma (Sparks, 1980). The possibility that structures other than smooth muscle cells, notably the endothelium, act as oxygen sensors is a further area for investigation. The emphasis here will be on studies relating the metabolic supply of smooth muscle and its contractile activity. 

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