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Am J Physiol Regul Integr Comp Physiol 290: R96-R104, 2006; doi:10.1152/ajpregu.00434.2005
0363-6119/06 $8.00
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Cardiovascular-Kidney Interactions in Health and Disease

D5 dopamine receptor regulation of reactive oxygen species production, NADPH oxidase, and blood pressure

Zhiwei Yang,1,2,3 Laureano D. Asico,2 Peiying Yu,2 Zheng Wang,2 John E. Jones,2 Crisanto S. Escano,2 Xiaoyan Wang,2 Mark T. Quinn,4 David R. Sibley,5 Guillermo G. Romero,6 Robin A. Felder,7 and Pedro A. Jose2,3

1Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) and Peking Union Medical College (PUMC), Beijing, China; 2Department of Pediatrics, 3Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, D.C.; 4Department of Veterinary Molecular Biology, Montana State University, Bozeman, Montana; 5National Institute of Neurological Disorders and Stroke, Bethesda, Maryland; 6Dept. of Pharmacology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, 7Department of Pathology, The University of Virginia Center for the Health Sciences, Charlottesville, Virginia

Submitted 20 June 2005 ; accepted in final form 12 September 2005

Activation of D1-like receptors (D1 and/or D5) induces antioxidant responses; however, the mechanism(s) involved in their antioxidant actions are not known. We hypothesized that stimulation of the D5 receptor inhibits NADPH oxidase activity, and thus the production of reactive oxygen species (ROS). We investigated this issue in D5 receptor-deficient (D5–/–) and wild-type (D5+/+) mice. NADPH oxidase protein expression (gp91phox, p47phox, and Nox 4) and activity in kidney and brain, as well as plasma thiobarbituric acid-reactive substances (TBARS) were higher in D5–/– than in D5+/+ mice. Furthermore, apocynin, an NADPH oxidase inhibitor, normalized blood pressure, renal NADPH oxidase activity, and plasma TBARS in D5–/– mice. In HEK-293 cells that heterologously expressed human D5 receptor, its agonist fenoldopam decreased NADPH oxidase activity, expression of one of its subunits (gp91phox), and ROS production. The inhibitory effect of the D5 receptor activation on NADPH oxidase activity was independent of cAMP/PKA but was partially dependent on phospholipase D2. The ability of D5 receptor stimulation to decrease ROS production may explain, in part, the antihypertensive action of D5 receptor activation.

hypertension


Address for reprint requests and other correspondence: P. A. Jose, Depts. of Pediatrics and Physiology and Biophysics, Georgetown Univ. Medical Center, 3800 Reservoir Rd., NW, Washington, DC 20007 (e-mail: pjose01{at}georgetown.edu)




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