Hypoxic vasodilatation: is an adenosine-prostaglandins- NO signalling cascade involved?
During hypoxia blood vessels in various tissues including skeletal muscle, heart and brain dilate in order to increase oxygen delivery to the hypoxic organ. The mechanism has long been of interest, but is still incompletely understood. Adenosine is known to be involved; it is released from cells during hypoxia in the metabolic regulation of blood flow (Berne, 1963). There is also evidence for an involvement of endothelial prostaglandins, nitric oxide (NO) and ATP (from which adenosine can be formed following ectoenzymatic degradation), and smooth muscle K(+) channels in hypoxia-induced vasodilatation (e.g. Busse et al. 1984; Messina et al. 1992). To date there have been few attempts to reconcile these different mechanisms.
D000241:Adenosine / Q000378:metabolism*; D000818:Animals; D000860:Hypoxia / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism*; D011453:Prostaglandins / Q000378:metabolism*; D015398:Signal Transduction; D014664:Vasodilation
D011453:Prostaglandins; D009569:Nitric Oxide; D000241:Adenosine