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

• DOI: 10.1073/pnas.171317998
• Publication Date: 2002-07-26T14:34:10Z
• Authors: Daqing Sun; Linda C. Samuelson; Tianxin Yang; Yuning Huang; Alex Paliege; Thom Saunders; Josie Briggs; Jurgen Schnermann
• Keywords: Tubuloglomerular feedback; Afferent arterioles; Macula densa; Juxtaglomerular apparatus; Adenosine A1 receptor

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