2007 JASN IMPACT FACTOR 7.111	HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP
advanced	CURRENT ISSUE	ARCHIVES	JASN Express	ONLINE SUBMISSION

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by HILL-KAPTURCZAK, N. Articles by TISHER, C. C. Search for Related Content PubMed PubMed Citation Articles by HILL-KAPTURCZAK, N. Articles by TISHER, C. C.

Angiotensin II-Stimulated Nitric Oxide Release from Porcine Pulmonary Endothelium Is Mediated by Angiotensin IV

NATHALIE HILL-KAPTURCZAK^*, MATTHIAS H. KAPTURCZAK^*, EDWARD R. BLOCK, JAWAHARLAL M. PATEL, TADEUSZ MALINSKI, KIRSTEN M. MADSEN^* and C. CRAIG TISHER^*

^* Department of Medicine, Division of Nephrology, Hypertension and Transplantation, University of Florida, Florida
Veterans Administration Medical Center, Gainesville, Florida
Department of Chemistry, and Institute of Biotechnology Oakland University, Rochester, MI.

Correspondence to Dr. Nathalie Hill-Kapturczak, Division of Nephrology, University of Florida, 1600 SW Archer Road, Box 100224, Gainesville, FL 32610. Phone: 352-392-4008; Fax: 352-392-3587; E-mail: Hillkn{at}medicine.ufl.edu

Abstract. In this study, a nitric oxide (NO) sensor was used to examine the ability of angiotensin II (AngII), AngIV, and bradykinin (Bk) to stimulate NO release from porcine pulmonary artery (PPAE) and porcine aortic endothelial (PAE) cells and to explore the mechanism of the AngII-stimulated NO release. Physiologic concentrations of AngII, but not Bk, caused release of NO from PPAE cells. In contrast, Bk, but not AngII, stimulated NO release from PAE cells. AngII-stimulated NO release from PPAE cells required extracellular L-arginine and was inhibited by L-nitro-arginine methyl ester. AT₁ and AT₂ receptor inhibition had no affect on AngII-mediated NO release or activation of NO synthase (NOS). AngIV, and AngII metabolite with binding sites that are pharmacologically distinct from the classic AngII receptors, stimulated considerably greater NO release and greater endothelial-type constitutive NOS activity than the same amount of AngII. The AngIV receptor antagonist, divalinal AngIV, blocked both AngII- and AngIV-mediated NO release as well as NOS activation. The results demonstrate that AngIV and the AngIV receptor are responsible, at least in part, for AngII-stimulated NO release and the associated endothelium-dependent vasorelaxation. Furthermore, these results suggest that differences exist in both AngII- and Bk-mediated NO release between PPAE and PAE cells, which may reflect important differences in response to these hormones between vascular beds.

This article has been cited by other articles:

				A. Vinh, R. E. Widdop, G. R. Drummond, and T. A. Gaspari Chronic angiotensin IV treatment reverses endothelial dysfunction in ApoE-deficient mice Cardiovasc Res, January 1, 2008; 77(1): 178 - 187. [Abstract] [Full Text] [PDF]

				J. Zheng, Y. Wen, D.-b. Chen, I. M. Bird, and R. R. Magness Angiotensin II Elevates Nitric Oxide Synthase 3 Expression and Nitric Oxide Production Via a Mitogen-Activated Protein Kinase Cascade in Ovine Fetoplacental Artery Endothelial Cells Biol Reprod, June 1, 2005; 72(6): 1421 - 1428. [Abstract] [Full Text] [PDF]

				J. Zheng, I. M. Bird, D.-B. Chen, and R. R. Magness Angiotensin II regulation of ovine fetoplacental artery endothelial functions: interactions with nitric oxide J. Physiol., May 15, 2005; 565(1): 59 - 69. [Abstract] [Full Text] [PDF]

				H. Cai, Z. Li, S. Dikalov, S. M. Holland, J. Hwang, H. Jo, S. C. Dudley Jr., and D. G. Harrison NAD(P)H Oxidase-derived Hydrogen Peroxide Mediates Endothelial Nitric Oxide Production in Response to Angiotensin II J. Biol. Chem., December 6, 2002; 277(50): 48311 - 48317. [Abstract] [Full Text] [PDF]

				G. Vauquelin, Y. Michotte, I. Smolders, S. Sarre, G. Ebinger, A. Dupont, and P. Vanderheyden Cellular targets for angiotensin II fragments: pharmacological and molecular evidence Journal of Renin-Angiotensin-Aldosterone System, December 1, 2002; 3(4): 195 - 204. [Abstract] [PDF]

				R. K. HANDA Characterization and Signaling of the AT4 Receptor in Human Proximal Tubule Epithelial (HK-2) Cells J. Am. Soc. Nephrol., March 1, 2001; 12(3): 440 - 449. [Abstract] [Full Text]

				S. Chen, J. M. Patel, and E. R. Block Angiotensin IV-mediated pulmonary artery vasorelaxation is due to endothelial intracellular calcium release Am J Physiol Lung Cell Mol Physiol, November 1, 2000; 279(5): L849 - L856. [Abstract] [Full Text] [PDF]

				M. de Gasparo, K. J. Catt, T. Inagami, J. W. Wright, and Th. Unger International Union of Pharmacology. XXIII. The Angiotensin II Receptors Pharmacol. Rev., September 1, 2000; 52(3): 415 - 472. [Abstract] [Full Text] [PDF]

				R. K. HANDA Metabolism Alters the Selectivity of Angiotensin-(1-7) Receptor Ligands for Angiotensin Receptors J. Am. Soc. Nephrol., August 1, 2000; 11(8): 1377 - 1386. [Abstract] [Full Text]

				J. M. Patel, Y. D. Li, J. Zhang, C. H. Gelband, M. K. Raizada, and E. R. Block Increased expression of calreticulin is linked to ANG IV-mediated activation of lung endothelial NOS Am J Physiol Lung Cell Mol Physiol, October 1, 1999; 277(4): L794 - L801. [Abstract] [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673