Chronic inhibition of nitric oxide increases the collateral vascular responsiveness to vasopressin in portal hypertensive rats

Huang, Hui‐Chun; Wang, Sun-Sang; Chan, Che‐Chang; Lee, Fa-Yauh; Chang, Full‐Young; H, Lin; Hou, Ming‐Chih; Tai, Chun-Ching; Lai, I-Nien; Lee, Shou‐Dong

doi:10.1016/j.jhep.2003.10.010

Cited by 14 publications

(13 citation statements)

References 32 publications

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“…This is compatible with our finding that in partially portal vein‐ligated (PVL) rats, the splanchnic hyporesponsiveness to glypressin during acute hemorrhage could be ameliorated by NO blockade 16,17 . Regarding the experiments on portal‐systemic collaterals, it has been reported that chronic NO inhibition by N G ‐nitro‐L‐arginine methyl ester (L‐NAME) enhances the collateral vascular response to vasopressin in PVL rats 18 . However, most of the previous experiments were designed to induce portal hypertension by PVL; this model is characterized by extensive portal‐systemic collateral formation without significant liver parenchymal change 19 .…”

Section: Introductionsupporting

confidence: 89%

Vasopressin response and shunting modulation in cirrhotic rats by chronic nitric oxide inhibition

Wang¹,

Lee

Chang³

et al. 2008

J of Gastro and Hepatol

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Section: Introductionsupporting

confidence: 89%

Vasopressin response and shunting modulation in cirrhotic rats by chronic nitric oxide inhibition

Wang¹,

Lee

Chang³

et al. 2008

J of Gastro and Hepatol

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“…In addition, the role of NO in the development of pulmonary hypertension varies among different models of the disease [78]. Recently, Huang et al [79] have suggested that chronic NO inhibition ameliorates portal-systemic shunting and improves the collateral vascular responsiveness to arginine vasopressin in portal hypertensive rats.…”

Section: Role Of Nitric Oxide In Hypertensionmentioning

confidence: 99%

Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology

Tuteja

Chandra

Tuteja

et al. 2004

BioMed Research International

196

128

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Nitric oxide (NO) is an intra- and extracellular messenger that mediates diverse signaling pathways in target cells and is known to play an important role in many physiological processes including neuronal signaling, immune response, inflammatory response, modulation of ion channels, phagocytic defense mechanism, penile erection, and cardiovascular homeostasis and its decompensation in atherogenesis. Recent studies have also revealed a role for NO as signaling molecule in plant, as it activates various defense genes and acts as developmental regulator. In plants, NO can also be produced by nitrate reductase. NO can operate through posttranslational modification of proteins (nitrosylation). NO is also a causative agent in various pathophysiological abnormalities. One of the very important systems, the cardiovascular system, is affected by NO production, as this bioactive molecule is involved in the regulation of cardiovascular motor tone, modulation of myocardial contractivity, control of cell proliferation, and inhibition of platelet activation, aggregation, and adhesion. The prime source of NO in the cardiovascular system is endothelial NO synthase, which is tightly regulated with respect to activity and localization. The inhibition of chronic NO synthesis leads to neurogenic and arterial hypertensions, which later contribute to development of myocardial fibrosis. Overall, the modulation of NO synthesis is associated with hypertension. This review briefly describes the physiology of NO, its synthesis, catabolism, and targeting, the mechanism of NO action, and the pharmacological role of NO with special reference to its essential role in hypertension.

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“…The portal‐systemic collateral vasoconstrictive effect of AVP was not modified by chronic simvastatin treatment. This is in contrast to the remarkable effects of chronic NO or prostaglandin synthesis inhibition in portal hypertension, such as hyperdynamic circulation modulation and collateral vasoconstrictive response improvement 5,36–38 . Although statins enhance NO and prostacyclin synthesis, 11,12,18 under the pre‐existing portal hypertensive state with enhanced peripheral vascular NO and prostacyclin activities and vasodilation, further vascular effects exerted by simvastatin may be negligible.…”

Section: Discussionmentioning

confidence: 86%

Simvastatin effects on portal‐systemic collaterals of portal hypertensive rats

Wang

Lee

Chen

et al. 2010

J of Gastro and Hepatol

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Chronic inhibition of nitric oxide increases the collateral vascular responsiveness to vasopressin in portal hypertensive rats

Cited by 14 publications

References 32 publications

Vasopressin response and shunting modulation in cirrhotic rats by chronic nitric oxide inhibition

Vasopressin response and shunting modulation in cirrhotic rats by chronic nitric oxide inhibition

Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology

Simvastatin effects on portal‐systemic collaterals of portal hypertensive rats

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