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Am J Physiol Regul Integr Comp Physiol 281: R1362-R1367, 2001. First published September 21, 2001; doi:10.1152/ajpregu.00470.2001
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Vol. 281, Issue 5, R1362-R1367, November 2001

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

Russell Brown1, Anna Ollerstam1, Björn Johansson2, Ole Skøtt3, Samuel Gebre-Medhin4, Bertil Fredholm2, and A. Erik G. Persson1

1 Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, S-751 23 Uppsala; 2 Department of Physiology and Pharmacology, Karolinska Institute, S-171 77 Stockholm; 4 Department of Medical Biochemistry, University of Göteborg, S-405 30 Göteborg, Sweden; and 3 Department of Physiology and Pharmacology, University of Southern Denmark, DK-5000 Odense, Denmark

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 anesthetized knockout, wild-type, and heterozygous 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 with 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 from 0 to 35 nl/min. 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 milli-Goldblatt units (mGU)/ml] mice compared with the wild-type and A1R+/- mice (36.3 ± 8.5 and 34.1 ± 9.6 mGU/ml), respectively. The results demonstrate that adenosine acting on A1R is required for TGF and modulates renin release.

knockout mice; angiotensin; renin release; micropuncture


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