The role of carbon monoxide as a gasotransmitter in cardiovascular and metabolic regulation

Abstract

Carbon monoxide (CO) is produced endogenously through the oxidative catabolism of heme by heme oxygenase (HO). First described as a putative neuronal signaling messenger, CO is now also known to be involved in a variety of physiological and pathophysiological processes in the cardiovascular system, including regulating blood pressure, smooth muscle cell proliferation, anti-inflammatory, antiapoptotic, and anti-coagulation effects.COcontributes substantially to the protective effects ofHOenzymes as a mediator of cell and tissue protection. The diverse actions of this diatomic gas mainly depend on the stimulation of soluble guanylate cyclase, opening of BKCa channels as well as activation of mitogen-activated protein kinases, and/or Akt signaling pathways. The cellular and molecular consequences of CO signaling are only partially characterized and appear to differ depending on cell types and circumstances. This chapter provides an overview of the many roles CO plays as a gasotransmitter in the cardiovascular system.