| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Science Center, Albuquerque, New Mexico 87131-5218
Chronic hypoxia (CH) is associated
with both blunted agonist-induced and myogenic vascular reactivity,
possibly due to an enhanced production of heme oxygenase (HO)-derived
carbon monoxide (CO). However, the cellular location of the HO
responsible for these effects has not been clearly established.
Therefore, we examined the response to administration of the substrate
for HO, heme-L-lysinate (HLL), in endothelium-intact and
endothelium-denuded small mesenteric arteries from CH male
Sprague-Dawley rats. Mesenteric arteries were isolated and mounted on
glass cannulas, pressurized to 60 mmHg, and superfused with
physiological saline solution. All experiments were performed in the
presence of 100 µM
N
-nitro-L-arginine. The
vasodilator response to HLL or exogenous CO was examined. HLL
experiments were performed in the presence and absence of the HO
inhibitor zinc protoporphyrin IX (ZnPPIX). HLL administration resulted
in a dose-dependent vasodilator response that was abolished in the
presence of ZnPPIX or by endothelial removal. Exogenous CO produced a
vasodilator response that was independent of an intact endothelium.
Cellular localization of HO was verified through immunohistochemistry
in sections of the gut and aorta from CH and control animals. Staining
for HO-1, HO-2, and endothelial nitric oxide synthase was confined to
the endothelium. Thus we conclude that CO is a product of HO located within the endothelium.
vasodilation; hypoxia; zinc protoporphrin IX; isolated vessels
This article has been cited by other articles:
|
|
 |
|
  D. Sacerdoti, M. Bolognesi, M. Di Pascoli, A. Gatta, J. C. McGiff, M. L. Schwartzman, and N. G. Abraham Rat mesenteric arterial dilator response to 11,12-epoxyeicosatrienoic acid is mediated by activating heme oxygenase Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1999 - H2002. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. H. Beierwaltes Induction of Heme Oxygenase: Can It Really Reverse Hypertension? Hypertension, October 1, 2006; 48(4): 555 - 557. [Full Text] [PDF]
|
|
|
|
|
|
J. J. Andresen, N. I. Shafi, W. Durante, and R. M. Bryan Jr. Effects of carbon monoxide and heme oxygenase inhibitors in cerebral vessels of rats and mice Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H223 - H230. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Rebel, S. Cao, H. Kwansa, S. Dore, E. Bucci, and R. C. Koehler Dependence of acetylcholine and ADP dilation of pial arterioles on heme oxygenase after transfusion of cell-free polymeric hemoglobin Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1027 - H1037. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Resch, C. Zawinka, G. Weigert, L. Schmetterer, and G. Garhofer Inhaled Carbon Monoxide Increases Retinal and Choroidal Blood Flow in Healthy Humans Invest. Ophthalmol. Vis. Sci., November 1, 2005; 46(11): 4275 - 4280. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Govindaraju, H. Teoh, Q. Hamid, P. Cernacek, and M. E. Ward Interaction between endothelial heme oxygenase-2 and endothelin-1 in altered aortic reactivity after hypoxia in rats Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H962 - H970. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Gibbons and G. Farrugia The role of carbon monoxide in the gastrointestinal tract J. Physiol., April 15, 2004; 556(2): 325 - 336. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Naik and B. R. Walker Heme oxygenase-mediated vasodilation involves vascular smooth muscle cell hyperpolarization Am J Physiol Heart Circ Physiol, June 5, 2003; 285(1): H220 - H228. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
