Characterization of three inhibitors of endothelial nitric oxide synthase in vitro and in vivo

Characterization of three inhibitors of endothelial nitric oxide synthase in vitro and in vivo 1 Three analogues of l‐arginine were characterized as inhibitors of endothelial nitric oxide (NO) synthase by measuring their effect on the endothelial NO synthase from porcine aortae, on the vascular tone of rings of rat aorta and on the blood pressure of the anaesthetized rat. 2 NG‐monomethyl‐l‐arginine (l‐NMMA), N‐iminoethyl‐l‐ornithine (l‐NIO) and NG‐nitro‐l‐arginine methyl ester (l‐NAME; all at 0.1–100 μm) caused concentration‐dependent inhibition of the Ca2+‐dependent endothelial NO synthase from porcine aortae. 3 l‐NMMA, l‐NIO and l‐NAME caused an endothelium‐dependent contraction and an inhibition of the endothelium‐dependent relaxation induced by acetylcholine (ACh) in aortic rings. 4 l‐NMMA, l‐NIO and l‐NAME (0.03–300 mg kg−1, i.v.) induced a dose‐dependent increase in mean systemic arterial blood pressure accompanied by bradycardia. 5 l‐NMMA, l‐NIO and l‐NAME (100 mg kg−1, i.v.) inhibited significantly the hypotensive responses to ACh and bradykinin. 6 The increase in blood pressure and bradycardia produced by these compounds were reversed by l‐arginine (30–100 mg kg−1 i.v.) in a dose‐dependent manner. 7 All of these effects were enantiomer specific. 8 These results indicate that l‐NMMA, l‐NIO and l‐NAME are inhibitors of NO synthase in the vascular endothelium and confirm the important role of NO synthesis in the maintenance of vascular tone and blood pressure. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Pharmacology Wiley

Characterization of three inhibitors of endothelial nitric oxide synthase in vitro and in vivo

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Publisher
Wiley
Copyright
1990 British Pharmacological Society
ISSN
0007-1188
eISSN
1476-5381
DOI
10.1111/j.1476-5381.1990.tb14151.x
Publisher site
See Article on Publisher Site

Abstract

1 Three analogues of l‐arginine were characterized as inhibitors of endothelial nitric oxide (NO) synthase by measuring their effect on the endothelial NO synthase from porcine aortae, on the vascular tone of rings of rat aorta and on the blood pressure of the anaesthetized rat. 2 NG‐monomethyl‐l‐arginine (l‐NMMA), N‐iminoethyl‐l‐ornithine (l‐NIO) and NG‐nitro‐l‐arginine methyl ester (l‐NAME; all at 0.1–100 μm) caused concentration‐dependent inhibition of the Ca2+‐dependent endothelial NO synthase from porcine aortae. 3 l‐NMMA, l‐NIO and l‐NAME caused an endothelium‐dependent contraction and an inhibition of the endothelium‐dependent relaxation induced by acetylcholine (ACh) in aortic rings. 4 l‐NMMA, l‐NIO and l‐NAME (0.03–300 mg kg−1, i.v.) induced a dose‐dependent increase in mean systemic arterial blood pressure accompanied by bradycardia. 5 l‐NMMA, l‐NIO and l‐NAME (100 mg kg−1, i.v.) inhibited significantly the hypotensive responses to ACh and bradykinin. 6 The increase in blood pressure and bradycardia produced by these compounds were reversed by l‐arginine (30–100 mg kg−1 i.v.) in a dose‐dependent manner. 7 All of these effects were enantiomer specific. 8 These results indicate that l‐NMMA, l‐NIO and l‐NAME are inhibitors of NO synthase in the vascular endothelium and confirm the important role of NO synthesis in the maintenance of vascular tone and blood pressure.

Journal

British Journal of PharmacologyWiley

Published: Nov 1, 1990

References

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