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Adenosine, type 1 receptors: role in proximal tubule Na + reabsorption
Author(s) -
Welch W. J.
Publication year - 2015
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12413
Subject(s) - reabsorption , chemistry , medicine , endocrinology , proximal tubule , sodium–hydrogen antiporter , adenosine , natriuresis , receptor , diuresis , tubular fluid , renal physiology , kidney , convoluted tubule , sodium , biochemistry , biology , organic chemistry
Adenosine type 1 receptor (A 1 ‐ AR ) antagonists induce diuresis and natriuresis in experimental animals and humans. Much of this effect is due to inhibition of A 1 ‐ AR s in the proximal tubule, which is responsible for 60–70% of the reabsorption of filtered Na + and fluid. Intratubular application of receptor antagonists indicates that A 1 ‐ AR mediates a portion of Na + uptake in PT and PT cells, via multiple transport systems, including Na + /H + exchanger‐3 ( NHE 3), Na + / PO 4 − co‐transporter and Na + ‐dependent glucose transporter, SGLT . Renal microperfusion and recollection studies have shown that fluid reabsorption is reduced by A 1 ‐ AR antagonists and is lower in A 1 ‐ AR KO mice, compared to WT mice. Absolute proximal reabsorption ( APR ) measured by free‐flow micropuncture is equivocal, with studies that show either lower APR or similar APR in A 1 ‐ AR KO mice, compared to WT mice. Inhibition of A 1 ‐ AR s lowers elevated blood pressure in models of salt‐sensitive hypertension, partially due to their effects in the proximal tubule.