AJP - Renal AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 287: F753-F759, 2004. First published June 22, 2004; doi:10.1152/ajprenal.00423.2003
0363-6127/04 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
287/4/F753    most recent
00423.2003v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (19)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kawada, N.
Right arrow Articles by Wilcox, C. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kawada, N.
Right arrow Articles by Wilcox, C. S.

TP receptors regulate renal hemodynamics during angiotensin II slow pressor response

Noritaka Kawada,1 Kathryn Dennehy,1 Glenn Solis,1 Paul Modlinger,1 Rebecca Hamel,1 Julie T. Kawada,1 Shakil Aslam,1 Toshiki Moriyama,2 Enyu Imai,2 William J. Welch,1 and Christopher S. Wilcox1

1Cardiovascular Kidney Institute and Division of Nephrology and Hypertension, Georgetown University, Washington, DC 20007; and 2Division of Nephrology, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan

Submitted 3 December 2003 ; accepted in final form 15 June 2004

We investigated the hypothesis that thromboxane A2 (TxA2)-prostaglandin H2 receptors (TP-Rs) mediate the hemodynamic responses and increase in reactive oxygen species (ROS) to ANG II (400 ng·kg–1·min–1 sc for 14 days) using TP-R knockout (TP –/–) and wild-type (+/+) mice. TP –/– had normal basal mean arterial blood pressure (MAP) and glomerular filtration rate but reduced renal blood flow and increased filtration fraction (FF) and renal vascular resistance (RVR) and markers of ROS (thiobarbituric acid-reactive substances and 8-isoprostane PGF2{alpha}) and nitric oxide (NOx). Infusion of ANG II into TP +/+ increased ROS and thromboxane B2 (TxB2) and increased RVR and FF. ANG II infusion into TP –/– mice reduced ANG I and increased aldosterone but caused a blunted increase in MAP (TP –/–: +6 ± 2 vs. TP +/+: +15 ± 3 mmHg) and failed to increase FF, ROS, or TxB2 but increased NOx and paradoxically decreased RVR (–2.1 ± 1.7 vs. +2.6 ± 0.8 mmHg·ml–1·min–1·g–1). Blockade of AT1 receptor of TP –/– mice infused with ANG II reduced MAP (–8 mmHg) and aldosterone but did not change the RVR or ROS. In conclusion, during an ANG II slow pressor response, AT1 receptors activate TP-Rs that generate ROS and prostaglandins but inhibit NO. TP-Rs mediate all of the increase in RVR and FF, part of the increase in MAP, but are not implicated in the suppression of ANG I or increase in aldosterone. TP –/– mice have a basal increase in RVR and FF associated with ROS.

thromboxane A2-prostaglandin H2 receptor; isoprostane; hypertension; renal vascular resistance


Address for reprint requests and other correspondence: C. S. Wilcox, Division of Nephrology and Hypertension, Georgetown Univ. Medical Center, 3800 Reservoir Rd. NE, PHCF6003, Washington, DC 20007-2197 (E-mail: wilcoxch{at}geogetown.edu)




This article has been cited by other articles:


Home page
 CirculationHome page
J. Xu and M.-H. Zou
Molecular Insights and Therapeutic Targets for Diabetic Endothelial Dysfunction
Circulation, September 29, 2009; 120(13): 1266 - 1286.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
H. Francois, N. Makhanova, P. Ruiz, J. Ellison, L. Mao, H. A. Rockman, and T. M. Coffman
A role for the thromboxane receptor in L-NAME hypertension
Am J Physiol Renal Physiol, October 1, 2008; 295(4): F1096 - F1102.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
S. D. Crowley, C. W. Frey, S. K. Gould, R. Griffiths, P. Ruiz, J. L. Burchette, D. N. Howell, N. Makhanova, M. Yan, H.-S. Kim, et al.
Stimulation of lymphocyte responses by angiotensin II promotes kidney injury in hypertension
Am J Physiol Renal Physiol, August 1, 2008; 295(2): F515 - F524.
[Abstract] [Full Text] [PDF]

Home page
 NDT PlusHome page
J. Thachil
The implications of aspirin resistance in renal failure
NDT Plus, June 1, 2008; 1(3): 192 - 193.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
W. J. Welch, K. Patel, P. Modlinger, M. Mendonca, N. Kawada, K. Dennehy, S. Aslam, and C. S. Wilcox
Roles of vasoconstrictor prostaglandins, COX-1 and -2, and AT1, AT2, and TP receptors in a rat model of early 2K,1C hypertension
Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2644 - H2649.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
O. B. Vagnes, B. M. Iversen, and W. J. Arendshorst
Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA2/isoprostane production
Am J Physiol Renal Physiol, September 1, 2007; 293(3): F860 - F867.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
K. Sebekova, T. Eifert, A. Klassen, A. Heidland, and K. Amann
Renal Effects of S18886 (Terutroban), a TP Receptor Antagonist, in an Experimental Model of Type 2 Diabetes
Diabetes, April 1, 2007; 56(4): 968 - 974.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
Y.-L. Tain and C. Baylis
Dissecting the Causes of Oxidative Stress in an In Vivo Model of Hypertension
Hypertension, November 1, 2006; 48(5): 828 - 829.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
A. L. Opay, C. R. Mouton, J. J. Mullins, and K. D. Mitchell
Cyclooxygenase-2 inhibition normalizes arterial blood pressure in CYP1A1-REN2 transgenic rats with inducible ANG II-dependent malignant hypertension
Am J Physiol Renal Physiol, September 1, 2006; 291(3): F612 - F618.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
Z. Qi, H. Cai, J. D. Morrow, and M. D. Breyer
Differentiation of Cyclooxygenase 1- and 2-Derived Prostanoids in Mouse Kidney and Aorta
Hypertension, August 1, 2006; 48(2): 323 - 328.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
C. S. Wilcox
Oxidative stress and nitric oxide deficiency in the kidney: a critical link to hypertension?
Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2005; 289(4): R913 - R935.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
J. D. Imig, X. Zhao, C. Z. Zaharis, J. J. Olearczyk, D. M. Pollock, J. W. Newman, I.-H. Kim, T. Watanabe, and B. D. Hammock
An Orally Active Epoxide Hydrolase Inhibitor Lowers Blood Pressure and Provides Renal Protection in Salt-Sensitive Hypertension
Hypertension, October 1, 2005; 46(4): 975 - 981.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.