<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Opay, Allison L</style></author><author><style face="normal" font="default" size="100%">Mouton, Cynthia R</style></author><author><style face="normal" font="default" size="100%">Mullins, John J</style></author><author><style face="normal" font="default" size="100%">Mitchell, Kenneth D</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cyclooxygenase-2 inhibition normalizes arterial blood pressure in CYP1A1-REN2 transgenic rats with inducible ANG II-dependent malignant hypertension.</style></title><secondary-title><style face="normal" font="default" size="100%">American journal of physiology. Renal physiology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Physiol. Renal Physiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Angiotensin II</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals, Genetically Modified</style></keyword><keyword><style  face="normal" font="default" size="100%">Blood Pressure</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclooxygenase 1</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclooxygenase 2</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclooxygenase 2 Inhibitors</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytochrome P-450 CYP1A1</style></keyword><keyword><style  face="normal" font="default" size="100%">Glomerular Filtration Rate</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypertension, Malignant</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Meclofenamic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Sulfonamides</style></keyword><keyword><style  face="normal" font="default" size="100%">Vascular Resistance</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2006 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">291</style></volume><pages><style face="normal" font="default" size="100%">F612-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The present study was performed to determine the effects of cyclooxygenase (COX)-1 and COX-2 inhibition on blood pressure and renal hemodynamics in transgenic rats with inducible malignant hypertension [strain name: TGR(Cyp1a1Ren2)]. Male Cyp1a1-Ren2 rats (n = 7) were fed a normal diet containing the aryl hydrocarbon, indole-3-carbinol (I3C; 0.3%), for 6-9 days to induce malignant hypertension. Mean arterial pressure (MAP) and renal hemodynamics were measured in pentobarbital sodium-anesthetized Cyp1a1-Ren2 rats during control conditions, following administration of the COX-2 inhibitor nimesulide (3 mg/kg iv), and following administration of the nonspecific COX inhibitor meclofenamate (5 mg/kg iv). Rats induced with I3C had higher MAP than noninduced rats (n = 7; 188 +/- 6 vs. 136 +/- 4 mmHg, P &lt; 0.01). There was no difference in renal plasma flow (RPF) or glomerular filtration rate (GFR) between induced and noninduced rats. Nimesulide elicited a larger decrease in MAP in hypertensive rats (188 +/- 6 to 140 +/- 8 mmHg, P &lt; 0.01) than in normotensive rats (136 +/- 4 to 113 +/- 8 mmHg, P &lt; 0.01). Additionally, nimesulide decreased GFR (0.9 +/- 0.13 to 0.44 +/- 0.05 ml.min(-1).g(-1), P &lt; 0.05) and RPF (2.79 +/- 0.27 to 1.35 +/- 0.14 ml.min(-1).g(-1), P &lt; 0.05) in hypertensive rats but did not alter GFR or RPF in normotensive rats. Meclofenamate further decreased MAP in hypertensive rats (to 115 +/- 10 mmHg, P &lt; 0.05) but did not decrease MAP in normotensive rats. Meclofenamate did not alter GFR or RPF in either group. These findings demonstrate that COX-1- and COX-2-derived prostanoids contribute importantly to the development of malignant hypertension in Cyp1a1-Ren2 transgenic rats. The data also indicate that COX-2-derived vasodilatory metabolites play an important role in the maintenance of RPF and GFR following induction of malignant hypertension in Cyp1a1-Ren2 transgenic rats.</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16622181?dopt=Abstract</style></custom1></record></records></xml>