Effects of Free Radicals on Coronary Artery

Abstract

Coronary arteries supply blood to the heart and hence the control of coronary tone is pivotal to human survival. Reactive oxygen species (ROS) in specified amounts play an important role in normal metabolic and signalling processes. However, excess ROS can cause severe cardiovascular damage. For example, NO is produced by endothelium as a signal for relaxation. However, in an inflammatory response, NO from endothelium or macrophages can combine with superoxide to produce more deleterious peroxynitrite. Excess ROS have been associated with loss of coronary artery pliability – loss of contraction in some instances and relaxation in others. Atherosclerosis may also be considered an inflammatory response that leads to artery blockage, coronary disease and ischaemia-reperfusion. ROS produce various types of damage to ion channels and pumps and this damage is associated with vascular diseases such as atherosclerosis and hypertension. Endothelium and smooth muscle in the coronary artery are also affected differently by individual ROS. In fact, endothelium may act to protect the underlying smooth muscle against ROS. This review will give an overview of this field.

Effects of peroxynitrite on sarco/endoplasmic reticulum Ca2+ pump isoforms SERCA2b and SERCA3a

“…It is inhibited by peroxynitrite and its decomposition product hydrogen peroxide. To avoid such interference from peroxynitrite in the subsequent assays, after incubation for 10 min at 37°C, the peroxynitrite and any hydrogen peroxide produced from its decomposition was quenched by adding dithiothreitol (DTT) to a final concentration of 1 mM and placing the samples on ice (24,41,43). Ca 2ϩ uptake.…”

“…Most tissues, including vascular smooth muscle, express a splice of SERCA2 (SERCA2b), whereas the splice of SERCA3a (SERCA3a) is widely expressed in tissues such as vascular endothelium, tracheal epithelium, mast cells, and lymphoid cells (3,9,11,13,27,44). Reactive oxygen species (ROS) are needed for cellular processes such as mitochondrial function and cell signaling (6,17,26,41). However, excess ROS may accumulate in ischemia reperfusion and in vascular pathologies such as atherogenesis and inflammation (1,6,26,41).…”

“…Reactive oxygen species (ROS) are needed for cellular processes such as mitochondrial function and cell signaling (6,17,26,41). However, excess ROS may accumulate in ischemia reperfusion and in vascular pathologies such as atherogenesis and inflammation (1,6,26,41). They can produce vascular dysfunctions by causing oxidation of lipids and various proteins by peroxides, superoxide, and hydroxyl radicals.…”

Modulation of Prostaglandin Biosynthesis by Nitric Oxide and Nitric Oxide Donors

“…However, at the beginning of the new millennium, a number of questions regarding NO biology still remain unanswered, the most challenging and confusing problem being set by the ambivalent character of NO. Although being a critical signaling messenger involved in the regulation of a wide range of physiologic processes, NO also has the ability to turn into a major cytotoxic effector molecule that is involved in a number of pathophysiologic conditions and in the pathogenesis of a growing list of human diseases (Jeremy et al, 2002;Szabo, 2003;Walia et al, 2003). On a clinical viewpoint, such a paradoxical fate of NO is particularly troublesome when one considers manipulating NO availability as a potential therapeutic option in different pathologic conditions.…”

Sustained Contraction and Endothelial Dysfunction Induced by Reactive Oxygen Species in Porcine Coronary Artery

“…1,2) Disruption to one or more of these mechanisms is thought to be responsible for the pathogenesis of various diseases. [3][4][5][6] Of these mechanisms, XOD may be involved in the generation of ROS in the endothelium during ischemia and/or reperfusion.…”