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1 Department of Medical Pharmacology and Physiology and The Dalton Cardiovascular Research Center, University of Missouri - Columbia School of Medicine, Columbia, Missouri, United States
2 Department of Medical Pharmacology and Physiology and The Dalton Cardiovascular Research Center, University of Missouri - Columbia School of Medicine, Columbia, Missouri, United States; Department of Medical Pharmacology and Physiology and the Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States
3 Department of Medical Pharmacology and Physiology and The Dalton Cardiovascular Research Center, University of Missouri - Columbia School of Medicine, Columbia, Missouri, United States; Dept of Med - Pharmacology & Physiology, University of Missouri, Columbia Schl of Medicine, Columbia, Missouri, United States
* To whom correspondence should be addressed. E-mail: korthuisr{at}health.missouri.edu.
Vascular inflammation and enhanced production of angiotensin II (Ang II) are involved in the pathogenesis of hypertension and diabetes, disease states that predispose the afflicted individuals to ischemic disorders. Based on these observations, we postulated that Ang II may play a role promoting leukocyte rolling (LR) and adhesion (LA) in postcapillary venules after exposure of the small intestine to ischemia/reperfusion (I/R). Using an intravital microscopic approach in C57BL/6J mice, we showed that Ang II AT1 or AT2 receptor antagonism (with valsartan or PD123,319, respectively), inhibition of angiotensin converting enzyme (ACE) with captopril, or CGRP receptor blockade (CGRP8-37) prevented postischemic LR but did not influence I/R-induced LA. However, both postischemic LR and LA were largely abolished by concomitant AT1 and AT2 receptor blockade or chymase inhibition (with Y-40079). Additionally, exogenously administered Ang II increased LR and LA, effects that were attenuated by pretreatment with a CGRP receptor antagonist or an NADPH oxidase inhibitor (apocynin). Our work suggests that Ang II, formed by the enzymatic activity of ACE and chymase, plays an important role in inducing postischemic LR and LA, effects that involve engagement of both AT1 or AT2 receptors and may be mediated by CGRP and NADPH oxidase.
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