NG-methyl-L-arginine causes endothelium-dependent contraction and inhibition of cyclic GMP formation in artery and vein.

Gold, Michele E.; Wood, Keith S.; Byrns, Russell E.; Fukuto, Jon M.; Ignarro, Louis J.

doi:10.1073/pnas.87.12.4430

Cited by 62 publications

(38 citation statements)

References 34 publications

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“…N G -hydroxy-L-arginine (NOHA) was obtained from Cayman Chemicals (Ann Arbor, MI). S-nitroso-N-acetylpenicillamine (SNAP) was synthesized as described (7). S-(2-boronoethyl)-L-cysteine (BEC) was a generous gift from D. W. Christianson (Univ.…”

Section: Methodsmentioning

confidence: 99%

Elevated arginase I expression in rat aortic smooth muscle cells increases cell proliferation

Liu

Wu²,

Morris³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

139

109

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Arginase, which exists as the isoforms arginase I and II, catalyzes the hydrolysis of arginine to ornithine and urea. Ornithine is the principal precursor for production of polyamines, which are required for cell proliferation. Rat aortic smooth muscle cells (RASMC) contain constitutive arginase I, and arginase inhibitors cause inhibition of cell proliferation. The objective of this study was to determine whether the elevated expression of arginase I in RASMC causes increased cell proliferation. RASMC were stably transfected with either rat arginase I cDNA or a ␤-galactosidase control expression plasmid. Western blots and arginase enzymatic assays revealed high-level expression of cytosolic arginase I in arginase I-transfected RASMC. Moreover, this observation was associated with the increased production of urea and polyamines and higher rates of RASMC proliferation. The two selective inhibitors of arginase, N G -hydroxy-L-arginine and S-(2-boronoethyl)-Lcysteine, inhibited arginase and decreased the production of urea and polyamines in arginase I-transfected RASMC, all of which were associated with the inhibition of cell proliferation. This study demonstrates that elevated arginase I expression increases RASMC proliferation by mechanisms involving increased production of polyamines. These observations suggest that arginase I plays a potentially important role in controlling RASMC proliferation.nitric oxide ͉ vascular smooth muscle growth ͉ polyamines ͉ atherosclerosis

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Section: Methodsmentioning

confidence: 99%

Elevated arginase I expression in rat aortic smooth muscle cells increases cell proliferation

Liu

Wu²,

Morris³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

139

109

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“…Endothelial expression of Nox5 can potentiate contractile responses to phenylephrine (80), but this is more likely to be due to the direct scavenging of nitric oxide that is released from the endothelium to counterbalance changes in vascular tone (27,29). A prominent cardiovascular effect of Nox1, which is primarily expressed in vascular smooth muscle, is to potentiate the pressor response to angiotensin II (20,26).…”

Section: Smooth Musclementioning

confidence: 99%

Nox5 and the Regulation of Cellular Function

Fulton

2009

Antioxidants & Redox Signaling

137

142

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The NADPH oxidase (Nox) family of enzymes is comprised of seven members, Noxes 1-5 and the Duoxes 1 and 2. Nox5 was the last of the conventional Nox enzymes to be identified, and in comparison to its siblings, much less is known about its molecular regulation and even less regarding its functional significance. The loss of Nox5 from rodent genomes has contributed significantly to this deficit in knowledge, but recent discoveries have narrowed the gap. There are many differences between Nox5 and the other Nox isoforms including alternative splicing, transcriptional regulation, enzymatic control mechanisms, tissue distribution, and intracellular trafficking. The goal of this review is to outline recent advances in our knowledge of the genetic regulation, the molecular mechanisms governing its activity, and the functional significance of Nox5 in human physiology and pathophysiology. Antioxid. Redox Signal. 11, 2443-2452.

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“…Several L-arginine analogues have been developed as nitric oxide synthase inhibitors, for example, N0-monomethyl-L-arginine (L-NMMA), N-iminoethyl-L-ornithine (L-NIO), and N0-nitro-L-arginine, or its methyl ester (L-NAME), (Dubbin et al, 1990; Moore et al, 1990; Moncada et al, 1991); all these have been shown to inhibit NO biosynthesis and also endothelium-dependent responses in vitro and in vivo. In addition to inhibiting endotheliumdependent relaxations, L-arginine analogues can also cause endothelium-dependent contractions of isolated vascular rings (Gold et al, 1990), increases in coronary perfusion pressure in isolated perfused hearts of rabbit (Amezcua et al, 1989) and guinea-pig (Levi et al, 1990) and marked hypertension and regional vasoconstriction when administered to conscious rats (Gardiner et al, 1990;Moncada et al, 1991). These actions of L-NAME, and the other L-arginine derivatives, have been ascribed to prevention or inhibition of basal or stimulated EDRF (NO)-elicited activation of cytosolic guanylate cyclase.…”

Section: Introductionmentioning

confidence: 99%

The effects of perfusion rate and N^G‐nitro‐L‐arginine methyl ester on cirazoline‐ and KCl‐induced responses in the perfused mesenteric arterial bed of rats

Adeagbo¹,

Tabrizchi²,

Triggle³

1994

British J Pharmacology

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1 The purpose of this study was to characterize the effects of N0-nitro-L-arginine methyl ester (L-NAME) on the perfusion rate/pressure relations, and on the pressor responses induced to cirazoline and KC1 in isolated, perfused mesenteric arterial beds from normotensive and spontaneously hypertensive rats. 2 The basal perfusion pressure of arterial beds perfused with either physiological salt solution (PSS) or PSS containing 1% polyvinylpyrrolidone increased as the perfusion rate increased. L-NAME, in concentrations up to 100 .lM, failed to alter the basal pressure regardless of the perfusion rate and viscosity; however, at 5 gM, it potentiated cirazoline-induced vasoconstriction at each of the perfusion rates. 3 L-NAME but not D-NAME caused a leftward shift of cirazoline concentration-response curves with a marked increase in the maximal response. The potentiating action of L-NAME was abolished in arterial beds perfused with a Ca2"-free physiological salt solution and also in beds denuded of endothelium by an infusion of distilled water for 5 min. 4 In endothelium-intact and -denuded preparations, L-NAME potentiated KCl pressor responses; the endothelium-independent potentiation of KCl pressor activity was stereospecific, time-independent and was not prevented by the presence of dexamethasone (0.511M) in the perfusion medium. However, L-NAME failed to potentiate vasoconstriction obtained to KCl in arterial beds denervated by cold storage (4-5°C) for 2 days. 5 The absence of K+ in the perfusate did not inhibit the ability of L-NAME to potentiate aadrenoceptor-mediated pressor responses, and nor did L-NAME inhibit KCl-induced vasodilatation in preconstricted arteries. It was thus concluded that L-NAME does not affect Na+/K+-ATPase activity. 6 No differences in the potentiating ability of L-NAME on either cirazoline-or KCl-mediated pressor responses were apparent between normotensive Sprague Dawley (SD), Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. 7 Our data thus provide evidence that: the presence of a vasoconstrictor is required for basal nitric oxide (NO) release in the mesenteric arterial bed from either normotensive or spontaneously hypertensive rats; L-NAME causes potentiation of cirazoline-and KCl-induced vasoconstriction respectively by inhibiting endothelial and neuronal NO synthase(s). Furthermore, our data indicate that NO synthase activity is not impaired in the mesenteric arterial bed of spontaneously hypertensive rats.

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NG-methyl-L-arginine causes endothelium-dependent contraction and inhibition of cyclic GMP formation in artery and vein.

Cited by 62 publications

References 34 publications

Elevated arginase I expression in rat aortic smooth muscle cells increases cell proliferation

Elevated arginase I expression in rat aortic smooth muscle cells increases cell proliferation

Nox5 and the Regulation of Cellular Function

The effects of perfusion rate and N^G‐nitro‐L‐arginine methyl ester on cirazoline‐ and KCl‐induced responses in the perfused mesenteric arterial bed of rats

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NG-methyl-L-arginine causes endothelium-dependent contraction and inhibition of cyclic GMP formation in artery and vein.

Cited by 62 publications

References 34 publications

Elevated arginase I expression in rat aortic smooth muscle cells increases cell proliferation

Elevated arginase I expression in rat aortic smooth muscle cells increases cell proliferation

Nox5 and the Regulation of Cellular Function

The effects of perfusion rate and NG‐nitro‐L‐arginine methyl ester on cirazoline‐ and KCl‐induced responses in the perfused mesenteric arterial bed of rats

Contact Info

Product

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The effects of perfusion rate and N^G‐nitro‐L‐arginine methyl ester on cirazoline‐ and KCl‐induced responses in the perfused mesenteric arterial bed of rats