| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-5218
Carbon monoxide (CO) has been proposed to attenuate the vasoconstrictor response to local hypoxia that contributes to pulmonary hypertension. However, the segmental response to CO, as well as its mechanism of action in the pulmonary circulation, has not been fully defined. To investigate the hemodynamic response to exogenous CO, lungs from male Sprague-Dawley rats were perfused with physiological saline solution. Measurements were made of pulmonary arterial, venous, and capillary pressures. Lungs were constricted with the thromboxane mimetic U-46619. To examine the vasodilatory response to CO, 500 µl of CO-equilibrated physiological saline solution or vehicle were injected into the arterial line. Additionally, CO and vehicle responses were examined in the presence of the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 µM) or the larger conductance calcium-activated K+ (BKCa) channel blockers tetraethylammonium chloride (10 mM) and iberiotoxin (100 nM). CO administration decreased vascular resistance to a similar degree in both vascular segments. This vasodilatory response was completely abolished in lungs pretreated with ODQ. Furthermore, CO administration increased whole lung cGMP content, which was prevented by ODQ. Neither tetraethylammonium chloride nor iberiotoxin affected the CO response. We conclude that exogenous CO administration causes vasodilation in the pulmonary vasculature via a soluble guanylyl cyclase-dependent mechanism that does not likely involve activation of KCa channels.
isolated rat lungs; pulmonary hypertension; vascular resistance; heme oxygenase
This article has been cited by other articles:
|
|
 |
|
  C. J. Mingone, M. Ahmad, S. A. Gupte, J. L. Chow, and M. S. Wolin Heme oxygenase-1 induction depletes heme and attenuates pulmonary artery relaxation and guanylate cyclase activation by nitric oxide Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1244 - H1250. [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]
|
|
|
|
 |
|
 O. V. Evgenov, F. Ichinose, N. V. Evgenov, M. J. Gnoth, G. E. Falkowski, Y. Chang, K. D. Bloch, and W. M. Zapol Soluble Guanylate Cyclase Activator Reverses Acute Pulmonary Hypertension and Augments the Pulmonary Vasodilator Response to Inhaled Nitric Oxide in Awake Lambs Circulation, October 12, 2004; 110(15): 2253 - 2259. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Zhang, J. I. Kaide, L. Yang, H. Jiang, S. Quan, R. Kemp, W. Gong, M. Balazy, N. G. Abraham, and A. Nasjletti CO modulates pulmonary vascular response to acute hypoxia: relation to endothelin Am J Physiol Heart Circ Physiol, January 1, 2004; 286(1): H137 - H144. [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 |
