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- fphys.2013.00194 author2 "Turner, Clare M.".
- fphys.2013.00194 author3 "Sixma, Marije L.".
- fphys.2013.00194 author4 "Singer, Mervyn".
- fphys.2013.00194 author5 "Unwin, Robert".
- fphys.2013.00194 author6 "Tam, Frederick W. K.".
- fphys.2013.00194 date "2013-01-01".
- fphys.2013.00194 doi "10.3389/fphys.2013.00194".
- fphys.2013.00194 first "Nishkantha".
- fphys.2013.00194 isCitedBy Purinergic_signalling.
- fphys.2013.00194 isCitedBy Tubuloglomerular_feedback.
- fphys.2013.00194 journal "Frontiers in Physiology".
- fphys.2013.00194 last "Arulkumaran".
- fphys.2013.00194 pages "194".
- fphys.2013.00194 pmc "3725473".
- fphys.2013.00194 pmid "23908631".
- fphys.2013.00194 quote "Extracellular adenosine contributes to the regulation of GFR. Renal interstitial adenosine is mainly derived from dephosphorylation of released ATP, AMP, or cAMP by the enzyme ecto-5′-nucleotidase . This enzyme catalyzes the dephosphorylation of 5′-AMP or 5′-IMP to adenosine or inosine, respectively, and is located primarily on the external membranes and mitochondria of proximal tubule cells, but not in distal tubule or collecting duct cells . ATP consumed in active transport by the macula densa also contributes to the formation of adenosine by 5- nucleotidase . Extracellular adenosine activates A1 receptors on vascular afferent arteriolar smooth muscle cells, resulting in vasoconstriction and a reduction in GFR .".
- fphys.2013.00194 title "Purinergic signaling in inflammatory renal disease".
- fphys.2013.00194 volume "4".