This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Coceani, F. Search for Related Content PubMed PubMed Citation Articles by Coceani, F. Related Collections Remodeling Animal models of human disease Gene regulation Smooth muscle proliferation and differentiation Pulmonary circulation and disease

(Circulation Research. 2000;86:1184.)
© 2000 American Heart Association, Inc.

Editorials

Carbon Monoxide in Vasoregulation

The Promise and the Challenge

Flavio Coceani

From the Scuola Superiore S. Anna and Istituto di Fisiologia Clinica CNR, Pisa, Italy.

Correspondence to Dr Flavio Coceani, Scuola Superiore S. Anna, Via Carducci 40, 56127 Pisa, Italy. E-mail coceani@sssup.it

Key Words: carbon monoxide • oxygen • vasoregulation • pulmonary hypertension

	Introduction

 
Less than 10 years have elapsed since the possibility of carbon monoxide (CO) being a novel signaling agent was first discussed.¹ In this time, a wealth of data has accrued supporting this idea and providing the foundation for physiological and pathophysiological schemes. Originating from heme through the action of specific oxygenases (heme oxygenase [HO]), which are both inducible (HO-1) and constitutive (HO-2 and HO-3) in character, CO may be formed at rest and, to a greater degree, on exposure to a host of HO-1–directed stimuli (ie, hypoxia, hyperoxia, shear stress, pyrogens, and metals, among the pertinent ones).^{2 3} It then exerts several effects within and without the vasculature. Blood vessels, in particular, have a complete system for the generation of CO and may dilate under the influence of the agent.^{4 5 6} Their actual response, however, varies with the vascular bed, and there are also instances of vessels failing unexpectedly to respond. Of relevance here is the recent observation of CO being ineffective on the pulmonary circulation in the fetus⁷ and hence on a system reproducing well, with a naturally high resistance, the condition of the hypertensive adult. The issue of apparent inconsistencies in CO action is intertwined with questions about the identity of the target for the compound. By analogy with nitric oxide (NO), the guanylate cyclase/cGMP system is commonly, and perhaps too hastily, regarded as the only messenger for CO inside cells, notwithstanding the relatively low affinity of the enzyme for the agent and the reported unresponsiveness of certain vessels. However, . . . [Full Text of this Article]

This article has been cited by other articles:

				W. Xuan, F.-Y. Zhu, S. Xu, B.-K. Huang, T.-F. Ling, J.-Y. Qi, M.-B. Ye, and W.-B. Shen The Heme Oxygenase/Carbon Monoxide System Is Involved in the Auxin-Induced Cucumber Adventitious Rooting Process Plant Physiology, October 1, 2008; 148(2): 881 - 893. [Abstract] [Full Text] [PDF]

				S. Oberle, A. Abate, N. Grosser, A. Hemmerle, H. J. Vreman, P. A. Dennery, H. T. Schneider, D. Stalleicken, and H. Schroder Endothelial Protection by Pentaerithrityl Trinitrate: Bilirubin and Carbon Monoxide as Possible Mediators Experimental Biology and Medicine, May 1, 2003; 228(5): 529 - 534. [Abstract] [Full Text] [PDF]

				J. H. Jaggar, C. W. Leffler, S. Y. Cheranov, D. Tcheranova, S. E, and X. Cheng Carbon Monoxide Dilates Cerebral Arterioles by Enhancing the Coupling of Ca2+ Sparks to Ca2+-Activated K+ Channels Circ. Res., October 4, 2002; 91(7): 610 - 617. [Abstract] [Full Text] [PDF]

				B. L. Graham, J. T. Mink, and D. J. Cotton Effects of Increasing Carboxyhemoglobin on the Single Breath Carbon Monoxide Diffusing Capacity Am. J. Respir. Crit. Care Med., June 1, 2002; 165(11): 1504 - 1510. [Abstract] [Full Text] [PDF]