Platelets and Cardioprotection: The Role of Nitric Oxide and Carbon Oxide

Abstract

Nitric oxide (NO) and carbon monoxide (CO) represent a pair of biologically active gases with an increasingly well-defined range of effects on circulating platelets. These gases interact with platelets and cells in the vessels and heart and exert fundamentally similar biological effects, albeit through different mechanisms and with some peculiarity. Within the cardiovascular system, for example, the gases are predominantly vasodilators and exert antiaggregatory effects, and are protective against damage in myocardial ischemia-reperfusion injury. Indeed, NO is an important vasodilator acting on vascular smooth muscle and is able to inhibit platelet activation. NO reacts with superoxide anion (O2(−•)) to form peroxynitrite (ONOO(−)), a nitrosating agent capable of inducing oxidative/nitrative signaling and stress both at cardiovascular, platelet, and plasma levels. CO reduces platelet reactivity, therefore it is an anticoagulant, but it also has some cardioprotective and procoagulant properties. This review article summarizes current knowledge on the platelets and roles of gas mediators (NO, and CO) in cardioprotection. In particular, we aim to examine the link and interactions between platelets, NO, and CO and cardioprotective pathways.

Oxidative Stress in Sepsis: A Focus on Cardiac Pathology

“…On the other hand, the synthesis of ONOO − during sepsis is a clear expression of tissue damage resulting from the cytotoxic effect of oxidative stress: (i) ONOO − and its derivatives with intracellular localization can oxidize target molecules, through direct or species-mediated action radicals; (ii) ONOO − promotes the formation of nitrogen dioxide (NO 2 ), supporting redox reactions with the consequent formation of nitrate species, such as NT; (iii) ONOO − interacts with nucleic acids, giving rise to 8-hydroxydeoxyguanosine [ 30 , 31 ].…”

Current Strategies to Guide the Antiplatelet Therapy in Acute Coronary Syndromes

“…An intact endothelium prevents thrombus formation mainly by the release of nitric oxide (NO) and prostacyclin (PGI2), the two major physiological antiplatelet agents [7][8][9]. The antiplatelet properties of NO and PGI2 depend on their ability to activate the cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) [10] and the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) [11,12] pathways, respectively.…”

Respiratory RNA viruses: Molecular mechanisms of viral replication and pathogenicity

“…eNOS is normally expressed in vascular endothelial cells, and its mediated production of NO can diffuse into smooth muscle cells, activate soluble guanylate cyclase (sGC) to produce cyclic guanosine monophosphate (cGMP), and activate protein kinase G (PKG), which phosphorylates myosin light chain kinase (MLCK), thereby relaxing the smooth muscle and leading to vasodilation (Arnold et al, 1977;Ataei Ataabadi et al, 2020;Ma et al, 2023). In addition, NO produced by eNOS has physiological functions such as inhibition of platelet aggregation and adhesion, inhibition of leukocyte adhesion and vascular inflammation, inhibition of smooth muscle cell proliferation, anti-atherosclerosis, etc., which are important for maintaining the normal function of the cardiovascular system (Förstermann and Sessa, 2012;Russo et al, 2023). nNOS regulates neurotransmitter release via the NO-NOsCG-cGMP signaling pathway and is also involved in the regulation of sympathetic nerves.…”