Nitric Oxide: An Attractive Signalling Molecule.

Endothelial Nitric Oxide Synthase: Correlation with Histologic Grade, Lymph Node Status and Estrogen Receptor Expression in Human Breast Cancer

“…Alternatively, it may be due to a balance between NOS activity by the different NOS isoforms, as the two subtypes of NOS, inducible and constitutive, are differentially regulated and function separately. Possibly, eNOS may act as a signal transduction mechanism [1] and iNOS may mediate several cytotoxic and cytostatic effects of the immune system [4,14].…”

“…Nitric oxide (NO), an inorganic free radical gas, has been shown to be a signalling molecule in many systems including nervous, vascular and immune systems [1]. It is a product of the nitric oxide synthase (NOS) family of isoenzymes, which convert L-arginine to Lcitrulline and nitric oxide [2].…”

Chronic administration of adenosine A3 receptor agonist and cerebral ischemia: neuronal and glial effects

“…Neurons, astrocytes, perivascular nerves, and the endothelium of cerebral vasculature have been shown to form nitric oxide (NO) during cerebral ischemia (Endoh et al, 1994;Kato et al, 1994;Loesch et al, 1994;Nakashima et al, 1995;Sparrow, 1995). However, while the activity of the constitutive NO synthase may be increased during ischemia (Dawson et al, 1991;Nagafuji et al, 1995), several studies have shown that its maximal stimulation apparently takes place at intracellular concentrations of Ca 2+ that are well below those encountered during cerebral ischemia (Knowles et al, 1989;Silver and Erecinska, 1990; see also the review by Aoki et al, 1995). Moreover, expression of the calciumrcalmodulin-dependent constitutive form of NO synthase appears to depend largely on small transients of intracellular Ca 2+ (Aoki et al, 1995).…”

“…However, while the activity of the constitutive NO synthase may be increased during ischemia (Dawson et al, 1991;Nagafuji et al, 1995), several studies have shown that its maximal stimulation apparently takes place at intracellular concentrations of Ca 2+ that are well below those encountered during cerebral ischemia (Knowles et al, 1989;Silver and Erecinska, 1990; see also the review by Aoki et al, 1995). Moreover, expression of the calciumrcalmodulin-dependent constitutive form of NO synthase appears to depend largely on small transients of intracellular Ca 2+ (Aoki et al, 1995). The inducible isoform of NO synthase, on the other hand, is independent of Ca 2+ transients (Dalkara et al, 1994;Sparrow, 1995) and, furthermore, late and sustained release of nitric oxide may be the result of enhanced expression of inducible NO synthase.…”

Arginine Administration Reduces Hydrogen Peroxide in Ischemia-reperfusion Endothelium of Rats.

“…In the process of tissue transplanation and vascular anastomosis, the IR injury induced by OFR is a critical problem [12]. Nitric oxide (NO) is a gaseous free radical and also a gaseous signal molecule, which participates in the regulation of vascular tone, platelet aggregation, leukocyte adhesion, synaptic transmission and cytostatic/cytotoxic actions of macrophages [2,12]. NO synthesis is catalyzed by a family of NO synthase (NOS) [9], which utilize L-Arg, oxygen and NADPH as substrates, and FAD, FMN, calmodulin and tertrahydrobiopterin as cofactors [10].…”