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NO synthase inhibitor

It has been proposed that NO mediates the myocardial depression associated with sepsis (F6, L14). NO synthesis induced by endotoxin blunts beta-adrenergic responsiveness (B2). In vivo, the use of NO synthase inhibitors led to conflicting results (M26), with a general decreased cardiac output and oxygen delivery being observed. NO synthase inhibition improved left ventricular contractility in endo-toxemic pigs but also increased ventricular afterloads, which ultimately is detrimental to cardiac function (H20). Possible sources of NO in the heart may be the vascular cells, the endothelial cells, and the cardiac myocytes (P6). [Pg.74]

NOx levels are increased in plasma and urine of septic animals. Many nonse-lective NO synthase inhibitors (e.g., L-NMMA) are used in several models with experimental induced sepsis (S40). In most studies it was shown that the cardiovascular abnormalities associated with sepsis were reversed, increasing blood pressure and systemic vascular resistance (F7, K9, M26, N5), together with a improvement in renal function (B42, H24). Also, selective inhibition of iNOS prolonged survival in septic rats (A7). [Pg.75]

Ribeiro, A. C. Kapas, L. (2003). Intra-suprachiasmatic nucleus (SCN) microinjection of a nitric oxide (NO) donor and NO synthase inhibitor affects sleep in rats. [Pg.334]

FIGURE 29.3 Analog of vitamin E-containing the a-tocopheryl moiety and the NO synthase inhibitor pharmacophore. [Pg.854]

Luminol semiquinone is further oxidized to luminol endoperoxide, which elicited CL at decomposition. It should be added that in our experiments peroxynitrite-stimulated luminol CL in cells was enhanced in the presence of the NO synthase substrate L-arginine and sharply diminished in the presence of NO synthase inhibitors. Thus, the application of substrates and inhibitors of NO synthases may discriminate luminol-amplified CL stimulated by superoxide and peroxynitrite. [Pg.972]

NO is recognized as a mediator of bone cell metabolism, where it regulates osteoblast and osteoclast activity [141-143]. Osteoporosis, which frequently occurs in postmenopausal women, is a systemic skeletal disease associated with abnormal bone resorption. Addition of NO or NO donors to osteoclasts in vitro results in a reduction in bone resorption, whereas NO synthase inhibitors increase bone resorption, both in vitro and in vivo. Further research has shown that NO reduces bone resorption, via inhibition of the cysteine protease cathepsin K, which is believed to be a key protease in bone resorption. Most of the NO donors, i.e., nitroglycerin, 3-... [Pg.23]

Attention then turned to the mechanism of glutamate-induced neurotoxicity in the brain. Evidence was provided that NO mediates glutamate neurotoxicity in primary cortical cultures (Dawson et ai, 1991). NO synthase inhibitors and hemoglobin prevented NMDA- and glutamate-induced neurotoxicity on the other hand, L-arginine reversed the effect of NO synthase inhibitors, and sodium nitroprusside (which decomposes to NO) caused neurotoxicity that paralleled cyclic GMP formation. In the cerebral cortex, NO synthase immunoreactivity was found to be confined to a discrete population of aspiny neurons comprising... [Pg.125]

Potential of NO Donors and NO Synthase Inhibitors for the Treatment of Pain... [Pg.555]

Studies to elucidate the functional role of NO have used inhibitors of NO synthase such as L-NAME and L-NMMA (see below). Systemic and intrathecal injections of NO synthase inhibitors have been shown to reduce noxious responses to formalin and carrageenan-induced hyperalgesia (Sakurada et al., 2001). Furthermore, NO-induced mechanical hyperalgesia has been reported to be mediated by supraspinal centers and does not occur in in vitro preparations of the spinal cord. [Pg.560]

Carry, J.-C., Damour, D., Guyon, C., Mignani, S., Bacque, E., Bigot, A (Aventis Pharma) 2-Aminothiazoline derivatives and their use as NO-synthase inhibitors, WO 0194325. [Pg.563]

Pettipher, E. R., Hibbs, T. A., Smith, M. A., Griffiths, R. J. Analgesic activity of 2-amino-4-methylpyridine, a novel NO synthase inhibitor, Inflamm. Res. 1997, 46, S135-S136. [Pg.565]

We have recently analysed the effects of an oral dose of quercetin, the most abundant dietary flavonoid, on the hypertension, oxidant status and renal, cardiac and vascular alterations induced in rats by chronic inhibition of NO synthesis with N-nitro L-arginine methylester (L-NAME). Administration of this NO synthase inhibitor to rats for six weeks induced a progressive increase in systolic blood pressure, but concomitant administration of an oral daily dose of quercetin (10 mg Kg 1) inhibited the development of hypertension induced by L-NAME (Duarte et al, 1999, Meth. Find. Exp. Clin. Pharmacol. 21 (suppl. A), 40). Moreover, when... [Pg.595]

Homocysteine decreases the bioavailability of nitrous oxide (NO) via a mechanism involving glutathione peroxidase (37). Tawakol et al. (38) reported that hyperhomocysteinemia is associated with impaired endothelium-dependent vasodilation in humans. Homocysteine impairs the NO synthase pathway both in cell culture (39) and in monkeys with hyperhomocysteinemia, by increasing the levels of asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhibitor (40). Elevation of ADMA may mediate endothelial dysfunction during experimental hyperhomocysteinemia in humans (41). However, Jonasson et al. (42) did not find increased ADMA levels in patients with coronary heart disease and hyperhomocysteinemia, nor did vitamin supplementation have any effect on ADMA levels in spite of substantial plasma tHcy reduction,... [Pg.179]

I CAM-1, VCAM-1, and endothelin-1 concentrations were significantly greater in men with ED and no cardiovascular disease symptoms compared to men without ED (24). Asymmetric demethyl arginine (ADMA) is an endogenous competitive nitric oxide (NO) synthase inhibitor and is an independent risk marker for cardiovascular disease impairing the L-arginine-NO pathway. Recent studies have found elevated levels of ADMA in men with ED and CAD (25 — 27). [Pg.506]

NO has been implicated in mediating the release of neurotransmitter/neuro-modulators such as substance P or glutamate (Meller and Gebhart, 1993). In addition, glial activation and cytokine production are found to be induced by NO (Guo et al., 2007 Holguin et al., 2004). The role of NO in activated astrocyte-induced glial cytokines after i.t. injection of M3G was examined by using the NO synthase inhibitor L-NAME. In mice treated with M3G, L-NAME was also very... [Pg.213]

Effects on antioxidant enzymes. Along with anti-radical effects camosine can influence enzymes which activity is connected directly or indirectly to free radical metabolism. Camosine and other CRC may work as NO synthase inhibitors in muscles [54]. Low concentrations of camosine (until 2.5 mM) can activate rabbit platelets 5 -lipoxygenase, whereas higher concentrations inhibit it [55]. Camosine, homocamosine or anserine (15-25 pM) inhibit rat brain tirosine hydroxylase by 50% at very low concentrations [56]. It was demonstrated recently that camosine may protect SOD from ROS attack under in vitro [57], and in vivo (our unpublished data) oxidative stress. [Pg.208]

Therapeutic Hbs such as DCLHb potentially are unique hemodiluents in that in addition to reducing viscosity, cerebral ischemic injury may also be reduced by the maintenance of oxygen delivery by the tHb and by the inactivation of nitric oxide (NO). This hypothesis was supported by the results of a study of cerebral ischemic injury in rats in which the effects of DCLHb infusion were compared to those of DCLHb infusion with l-NAME (an NO synthase inhibitor) or... [Pg.364]

NO pathway manipulation affects CSA chronic nephrotoxicity. Supplementation of the NO substrate, -L-arginine, amehorated whereas use of -L-NAME, a NO synthase inhibitor, aggravated tubulointerstitial fibrosis [102]. Likewise, CSA-induced up-regulation of TGF-(31, plasminogen activator inhibitor-1 and deposition of extracellular matrix components were aggravated by NO blockade and ameliorated by NO enhancement [510]. [Pg.634]

A primary mediator that was demonstrated to participate in meningitis-induced BBB dismption is nitric oxide (NO). NO is produced in response to exposure to bacterial endotoxins by the host endothelial cells. In an animal model of lipopolysaccharide-induced meningitis, BBB dismption and NO production sites in the brain co-local-ized, and NO-synthase inhibitors reduced the meningeal-associated alterations in BBB permeability. NO is likely produced by astrocytes, and it decreases endothe-lin-1 secretion by brain microvessel endothelial cells. ... [Pg.145]


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See also in sourсe #XX -- [ Pg.555 , Pg.558 , Pg.560 ]




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