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Am J Physiol Renal Physiol 275: F922-F927, 1998;
0363-6127/98 $5.00
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Vol. 275, Issue 6, F922-F927, December 1998

Inhibition of adenosine-1 receptor-mediated preglomerular vasoconstriction in AT1A receptor-deficient mice

Timothy Traynor1, Tianxin Yang1, Yuning G. Huang1, Lois Arend1, Michael I. Oliverio3, Thomas Coffman3, Josie P. Briggs1,2, and Jürgen Schnermann1

1 Departments of Physiology and Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109; 2 Division of Kidney, Urological, and Hematological Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and 3 Department of Medicine, Duke University, Durham, North Carolina 27710

The effect of the adenosine type 1 receptor agonist N6-cyclohexyladenosine (CHA) on glomerular vascular reactivity was studied in male angiotensin II type 1A (AT1A) receptor knockout mice (9). Vascular reactivity was assessed as the response of stop-flow pressure (PSF) to infusion of CHA into loops of Henle using micropuncture techniques. In AT1A +/+ mice at ambient arterial blood pressure (96.7 ± 2.8 mmHg), the presence of CHA (10 -5 M) in the perfusate increased PSF responses from 6.8 ± 0.6 to 14.3 ± 0.9 mmHg when the loop of Henle of the index nephron was perfused and from 0.7 ± 0.3 to 12.3 ± 1.0 mmHg when the loop of an adjacent nephron was perfused. At reduced arterial blood pressure (82.8 ± 1.3 mmHg), index nephron perfusion with CHA increased PSF responses from 4.5 ± 0.3 to 9.4 ± 0.4 mmHg. In AT1A -/- mice with a mean arterial blood pressure of 80 ± 1.9 mmHg, CHA increased PSF responses only from 0.1 ± 0.3 to 3.6 ± 0.54 mmHg during index nephron perfusion and from 0.25 ± 0.2 to 2.7 ± 0.55 mmHg during adjacent nephron perfusion, significantly less than in wild-type animals (P < 0.001). Responses to CHA were intermediate in AT1A +/- mice. Thus AT1A receptor knockout mice show a markedly reduced constrictor response to CHA both in the presence and absence of simultaneous activation of the tubuloglomerular feedback system. These data support the notion of a functional interaction between adenosine and angiotensin II in the regulation of afferent arteriolar tone.

micropuncture; mouse; angiotensin II type 1A receptor; gene knockout; tubuloglomerular feedback; adenosine type 1 receptor


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