RGD Reference Report - Mediation of tubuloglomerular feedback by adenosine: evidence from mice lacking adenosine 1 receptors. - Rat Genome Database

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Mediation of tubuloglomerular feedback by adenosine: evidence from mice lacking adenosine 1 receptors.

Authors: Sun, D  Samuelson, LC  Yang, T  Huang, Y  Paliege, A  Saunders, T  Briggs, J  Schnermann, J 
Citation: Sun D, etal., Proc Natl Acad Sci U S A 2001 Aug 14;98(17):9983-8.
RGD ID: 1300260
Pubmed: PMID:11504952   (View Abstract at PubMed)
PMCID: PMC55564   (View Article at PubMed Central)
DOI: DOI:10.1073/pnas.171317998   (Journal Full-text)

Adenosine is a determinant of metabolic control of organ function increasing oxygen supply through the A2 class of adenosine receptors and reducing oxygen demand through A1 adenosine receptors (A1AR). In the kidney, activation of A1AR in afferent glomerular arterioles has been suggested to contribute to tubuloglomerular feedback (TGF), the vasoconstriction elicited by elevations in [NaCl] in the macula densa region of the nephron. To further elucidate the role of A1AR in TGF, we have generated mice in which the entire A1AR coding sequence was deleted by homologous recombination. Homozygous A1AR mutants that do not express A1AR mRNA transcripts and do not respond to A1AR agonists are viable and without gross anatomical abnormalities. Plasma and urinary electrolytes were not different between genotypes. Likewise, arterial blood pressure, heart rates, and glomerular filtration rates were indistinguishable between A1AR(+/+), A1AR(+/-), and A1AR(-/-) mice. TGF responses to an increase in loop of Henle flow rate from 0 to 30 nl/min, whether determined as change of stop flow pressure or early proximal flow rate, were completely abolished in A1AR(-/-) mice (stop flow pressure response, -6.8 +/- 0.55 mmHg and -0.4 +/- 0.2 in A1AR(+/+) and A1AR(-/-) mice; early proximal flow rate response, -3.4 +/- 0.4 nl/min and +0.02 +/- 0.3 nl/min in A1AR(+/+) and A1AR(-/-) mice). Absence of TGF responses in A1AR-deficient mice suggests that adenosine is a required constituent of the juxtaglomerular signaling pathway. A1AR null mutant mice are a promising tool to study the functional role of A1AR in different target tissues.

Objects referenced in this article
Gene ADORA1 adenosine A1 receptor Homo sapiens
Gene Adora1 adenosine A1 receptor Mus musculus
Gene Adora1 adenosine A1 receptor Rattus norvegicus

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