Hypothesis: adenosine mediates hemodynamic changes in renal failure.
The decreased filtration fraction and glomerular filtration rate characteristic of renal failure could be produced, at least in part, by increased concentration of an endogenous substance which constricts afferent and dilates efferent arterioles. Adenosine satisfies several criteria: (a) exogenous adenosine and its precursors decrease filtration fraction and glomerular filtration rate; (b) the kidneys produce and release adenosine, and production and release are augmented during conditions associated with the induction of renal failure--hypoxia, ischemia, and renal vasoconstriction; (c) several substances known to antagonize adenosine-uptake processes in some cells, which could thereby increase extracellular adenosine concentration, not only have "adenosine-like" effects on the kidney but also induce and/or potentiate existing renal failure. A corollary of this hypothesis is that adenosine-receptor antagonists, such as the methylxanthines, should counteract the hemodynamic changes characteristic of renal failure. It has been known for several years that aminophylline (1,3-dimethylxanthine ethylenediamine) increases the filtration fraction and the glomerular filtration rate.
D000241:Adenosine / Q000097:blood*; D005919:Glomerular Filtration Rate; D006439:Hemodynamics; D006801:Humans; D007668:Kidney / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000097:blood*; D011956:Receptors, Cell Surface / Q000378:metabolism; D011983:Receptors, Purinergic; D012079:Renal Circulation; D012084:Renin-Angiotensin System
D011956:Receptors, Cell Surface; D011983:Receptors, Purinergic; D000241:Adenosine