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Carbon Monoxide — From Tool to Neurotransmitter
Published in David G. Penney, Carbon Monoxide, 2019
Nanduri R. Prabhakar, Robert S. Fitzgerald
It is becoming increasingly apparent that gases such as nitric oxide (NO) and CO function as neurotransmitters (Moneada et al., 1991; Snyder, 1992). They seem to satisfy many of the criteria proposed for a transmitter: ( 1 ) they are synthesized in the nervous system; (2) they are released by the cells; (3) exogenous application influences neuronal activity; and (4) blockade of their synthesis affects many neuronal functions. However, NO and CO are unconventional transmitters in certain aspects. Unlike the classical transmitters, they are not stored in synaptic vesicles, nor do they act on membrane-bound receptors. Instead, they are produced according to need, and once formed, rapidly diffuse out of the cell. The only known “receptor” for NO and CO in the post-synaptic site is the iron in the heme moiety of proteins such as the enzyme soluble guanylate cyclase.
The Microcirculation Physiome
Published in Joseph D. Bronzino, Donald R. Peterson, Biomedical Engineering Fundamentals, 2019
Aleksander S. Popel and Roland N. Pittman
synthase are divided into inducible NOS (iNOS or NOS2) and constitutive NOS (cNOS), based on their nondependent and dependent, respectively, control of activity from intracellular calcium/calmodulin. Constitutive NOS are further classied as neuronal NOS (nNOS or NOS1) and endothelial NOS (eNOS or NOS3). Nitric oxide plays an important role in both autocrine and paracrine manners in a myriad of physiological processes, including regulation of blood pressure and blood ow, platelet aggregation, and leukocyte adhesion. In smooth muscle cells, NO activates the enzyme soluble guanylate cyclase (sGC) that catalyzes the conversion of guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP), thus causing vasodilation [8]. Traditionally, eNOS has been considered the principal source of bioavailable microvascular NO under most physiological conditions. Evidence exists that nNOS expressed in nerve bers, which innervate arterioles, together with nNOS positive mast cells are also major sources of NO [46]. NO produced by endothelial cells diuses to vascular smooth muscle and to the owing blood, where it rapidly reacts with hemoglobin in RBCs and free hemoglobin present in pathological conditions, such as sickle cell disease, or during administration of free hemoglobin as a blood substitute. Other nonneuronal cell types, including cardiac and skeletal myocytes, also express nNOS. Direct measurements of NO concentration in the microcirculation with high spatial resolution have been performed with carbon ber microsensors [10] and optical dyes [46], although recent criticism has been directed to current measurements of NO in vivo [40]. In addition to its vasodilatory eect, NO also inhibits mitochondrial respiration by its interaction with cytochrome c oxidase [19]. Mathematical models of NO transport have been developed that describe the transport of NO synthesized by eNOS and nNOS in and around microvessels [88]. Other mechanisms have been proposed and are under intense scrutiny, for example, NO reacting with thiols in blood to form long-lived S-nitrosothiols (SNOs) with vasodilatory activity [1], and nitrite being a source of NO [91]. ere are signicant discrepancies between experimental data and theoretical results that await resolution [17,40]; the sources of microvascular bioavailable NO also need to be revealed.
The vasorelaxant effect of Canarium odontophyllum Miq. (Dabai) extract in rat thoracic aorta
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Dayang Fredalina Basri, Nur Sa'adah Abdul Rahman, Shafreena Shaukat Ali, Satirah Zainalabidin
Vascular endothelium which is located between the circulating blood and vascular smooth muscle plays an important role in regulating the vascular tone. Modulation of vascular tone by endothelium is mediated by the release of vasodilators (NO and prostacyclin) and vasoconstrictors such as endothelin and angiotensin II [17]. Relaxation in vascular smooth muscle can occur through the NO/cGMP pathway. In endothelial cell, the calcium-calmodulin complex stimulates NO synthase (NOS), which later activates NO formation from L-Arginine. NO then enters the smooth muscle cells and stimulates guanylate cyclase, which increases intracellular cyclic guanosine monophosphate (cGMP). The increased of the intracellular cGMP then stimulate cGMP dependent protein kinases leading to a decrease in the calcium concentrations in the smooth muscle cells, which causes its relaxation [18].
Effects of continuous and pulsatile flows generated by ventricular assist devices on renal function and pathology
Published in Expert Review of Medical Devices, 2018
Takuma Miyamoto, Jamshid H. Karimov, Kiyotaka Fukamachi
ARF may occur during severe episodes of hemoglobinuria. Persistent severe hemoglobinuria is also associated with substantial proximal tubule hemosiderin deposition. In a typical course of CF LVAD support, severe hemoglobinuria did not occur unless there were complications leading to hemolysis, such as device thrombosis. However, some amount of hemolysis occurs during CF LVAD support due to extraphysiologic shear stress. Rother et al. [50] proposed the existence of hemolysis-associated smooth muscle dystonia, vasculopathy, and endothelial dysfunction. Nitric oxide reacts with hemoglobin in an extremely fast and irreversible reaction that produces an inactive oxidation product nitrate (NO3) and methemoglobin. The authors propose that the release of hemoglobin during intravascular hemolysis results in excessive consumption of nitric oxide, subsequent reduction in guanylate cyclase activity, smooth muscle contraction, vasoconstriction, and platelet activation/aggregation. John et al. [51] investigated changes in the endothelial system in CF LVAD recipients. They found no significant differences in the number of circulating endothelial cells in either CF LVAD recipients or control patients (patients who underwent non-LVAD cardiac surgery) compared with those in the normal range. However, markers of endothelial activation (including vascular cell adhesion molecule-1, intercellular adhesion molecule, E-selectin, and tissue factor) were all significantly higher at baseline in CF LVAD recipients. All these markers further peaked on POD 7 and remained significantly elevated until POD 180. Nascimbene et al. [52] focused on microparticles. A persistent and systemic generation of microparticles can lead to a sustained pro-inflammatory and pro-coagulant state and can cause activation of the endothelium, which responds to microparticle-bound tissue factor. Phosphatidylserine plus microparticle levels were higher in patients at baseline than in healthy controls. After CF LVAD implantation, phosphatidylserine plus microparticle levels were high in patients at post-surgery baseline, at discharge after implantation, and at 3 months. Ahmad et al. [53] examined long-term changes in commonly measured laboratory parameters in 37 consecutive patients, aged 18 years and older, who required MCS with a CF LVAD. Median concentrations of neutrophil gelatinase-associated lipocalin – a diagnostic biomarker of early AKI, also considered a risk marker of atherosclerosis [54] – did not change significantly, despite concomitant decreases in Cre after CF LVAD support.