Mechanisms of rho kinase regulation of vascular reactivity following hemorrhagic shock in rats.

Mechanisms of rho kinase regulation of vascular reactivity following hemorrhagic shock in rats. Research Abstract Details 

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Mechanisms of rho kinase regulation of vascular reactivity following hemorrhagic shock in rats. Abstract Text:

Tao Li,Liangming Liu,Jiancang Liu,Jia Ming,Jing Xu,Guangming Yang,Yuan Zhang,Tao Li,Liangming Liu,Jiancang Liu,Jia Ming,Jing Xu,Guangming Yang,Yuan Zhang,

Our previous research showed that Rho kinase took part in the regulation of vascular hyporeactivity after shock. The objective of the present study was to investigate its mechanism. With isolated superior mesenteric artery (SMA) from hemorrhagic shock rats, we studied the relationship of Rho kinase regulating vascular reactivity to calcium sensitivity and myosin light chain phosphatase (MLCP) and myosin light chain kinase (MLCK). The vascular reactivity and calcium sensitivity of SMA were observed by measuring the contraction initiated by accumulative norepinephrine (NE) and calcium under depolarizing condition (120 mM K) with an isolated organ perfusion system. Hypoxia-treated vascular smooth muscle cells (VSMCs) were used to study the effects of Rho kinase on the activity of MLCP and MLCK and the phosphorylation of 20-kDa myosin light chain (MLC20). Myosin light chain (20 kDa) phosphorylation of VSMC in mesenteric artery was detected by immunoprecipitation and Western blotting. The activity of MLCP and MLCK was assayed by enzymatic catalysis. The contractile response of VSMC was measured by the ratio of accumulative infiltration of fluorescent isothiocyanate-conjugated bovine serum albumin through transwell. The results indicated that the vascular reactivity and calcium sensitivity of SMA to NE and calcium following hemorrhagic shock and the contractile response of VSMC to NE following hypoxia were significantly decreased. Angiotensin II (Ang-II), the Rho kinase stimulator, significantly improved hypoxia or hemorrhagic shock-induced decrease of vascular reactivity and calcium sensitivity. These effects of Ang-II on vascular reactivity were abolished by Y-27632, the specific Rho kinase inhibitor. Calyculin A, the MLCP inhibitor, further enhanced Ang-II-induced increase of calcium sensitivity, but ML-9, the MLCK inhibitor, had no effect. Further studies showed Ang-II reversed the hypoxia-induced increase of MLCP activity and increased the hypoxia-induced decrease of MLC20 phosphorylation in VSMC. It was suggested that Rho kinase played an important role in the regulation of vascular reactivity after hemorrhagic shock. The mechanisms may be related to its calcium sensitivity regulation. Rho kinase up-regulates calcium sensitivity of VSMC possibly through inhibiting the activity of MLCP and increasing the phosphorylation of MLC20.

Mechanisms of rho kinase regulation of vascular reactivity following hemorrhagic shock in rats. Publishing Authors By Initials

T Li,L Liu,J Liu,J Ming,J Xu,G Yang,Y Zhang,T Li,L Liu,J Liu,J Ming,J Xu,G Yang,Y Zhang,

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Mechanisms of rho kinase regulation of vascular reactivity following hemorrhagic shock in rats. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Shock (Augusta, Ga.)

VOLUME: 29

Page Numbers: 65-70

Journal Abbreviation: Shock

ISSN: 1073-2322

DAY: 4

MONTH: Jan

YEAR: 2008

Mechanisms of rho kinase regulation of vascular reactivity following hemorrhagic shock in rats. Information

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LANGUAGE: eng

NlmUniqueID: 9421564

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AFFILIATION: State Key Laboratory of Trauma, Burns and Combined Injury, The 2nd Department of Research Institute of Surgery, Daping Hospital, The Third Military Medical University, Chongqing, P.R. China.

Country: United States

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MEDLINETA: Shock

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