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Am J Physiol Regul Integr Comp Physiol (September 21, 2001). doi:10.1152/ajpregu.00470.2001
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Articles in PresS, published online ahead of print September 21, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00470.2001
Submitted on August 3, 2001
Accepted on August 9, 2001

Abolished tubuloglomerular feedback and increased plasma renin in adenosine A1 receptor deficient mice

Russell Brown1, Anna Ollerstam1, Bjorn Johansson2, Ole Skott3, Samuel Gebre-Medhin4, Bertil Fredholm2, and A. Erik G Persson1*

1 Medical Cell Biology, Uppsala University, Uppsala, Sweden
2 Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden
3 Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark
4 Medical Biochemistry, Goteborg University, Goteborg, Sweden

* To whom correspondence should be addressed. E-mail: anna.ollerstam{at}bmc.uu.se.

The hypothesis that adenosine acting on adenosine A1 receptors (A1R) regulates several renal functions and mediates tubuloglomerular feedback (TGF) was examined using A1R knockout mice. We anaesthetized knockout, wild-type and heterozygote mice and measured glomerular filtration rate, TGF response using the stop-flow pressure (Psf) technique and plasma renin concentration. The A1R knockout mice had an increased blood pressure compared to wild-type and heterozygote mice. Glomerular filtration rate was similar in all genotypes. Proximal tubular Psf was decreased from 36.7±1.2 to 25.3±1.6 mmHg in the A1R+/+ mice and from 38.1±1.0 to 27.4±1.1 mmHg in A1R+/- mice in response to an increase in tubular flow rate frpm 0 to 35 nl min-1. This response was abolished in the homozygous A1R -/- mice (from 39.1±4.1 to 39.2±4.5 mmHg). Plasma renin activity was significantly greater in the A1R knockout mice (74.2±14.3 mGU ml-1) mice compared to the wild type and A1R+/- mice (36.3±8.5 and 34.1±9.6 mGU ml-1), respectively. The results demonstrate that adenosine acting on A1R is required for TGF and modulates renin release.




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