1. The present review is concerned with the effects of acute systemic hypoxia on the gross vascular conductance of skeletal muscle (MVC) and on the behaviour of muscle microcirculation. 2. On the basis of experiments performed in the rat, it is argued that adenosine released from the vascular endothelium plays a major role in dilating muscle vasculature by acting on adenosine A(1) receptors. 3. The dilatation of the proximal arterioles is primarily important in increasing MVC and in limiting the fall in O-2 delivery to muscle. It is suggested that the action of adenosine on proximal arterioles is dependent on nitric oxide (NO) rather than mediated by NO, such that adenosine dilates the proximal arterioles via other mechanisms when synthesis of NO is blocked. 4. In contrast, dilatation of terminal arterioles, particularly in regions within muscle where the hypoxia is most severe, helps to improve the distribution of available O-2 , allowing muscle O-2 consumption to be maintained by increased O-2 extraction. It is concluded that the action of adenosine on terminal arterioles is mainly mediated by NO arising from stimulation of endothelial A(1) receptors. 5. Therefore, adenosine plays a major role in coordinating the behaviour of muscle vasculature such that the relationship between O-2 supply and O-2 demand can be optimized even when the O-2 content of the arterial blood is greatly reduced.
|Number of pages||7|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 1 Sep 2002|