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Hyperdynamic circulation in liver cirrhosis

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Hyperdynamic circulation in liver cirrhosis : desensitization of vasoconstrictive receptors by G protein-coupled receptor kinases. / Vashist, Yogesh; Semela, David; Dufour, Jean-François.

In: MED HYPOTHESES, Vol. 62, No. 1, 2004, p. 82-5.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Vashist, Y, Semela, D & Dufour, J-F 2004, 'Hyperdynamic circulation in liver cirrhosis: desensitization of vasoconstrictive receptors by G protein-coupled receptor kinases', MED HYPOTHESES, vol. 62, no. 1, pp. 82-5.

APA

Vashist, Y., Semela, D., & Dufour, J-F. (2004). Hyperdynamic circulation in liver cirrhosis: desensitization of vasoconstrictive receptors by G protein-coupled receptor kinases. MED HYPOTHESES, 62(1), 82-5.

Vancouver

Vashist Y, Semela D, Dufour J-F. Hyperdynamic circulation in liver cirrhosis: desensitization of vasoconstrictive receptors by G protein-coupled receptor kinases. MED HYPOTHESES. 2004;62(1):82-5.

Bibtex

@article{cf01dd8aa6cd4cec9aec8a4fe7560088,
title = "Hyperdynamic circulation in liver cirrhosis: desensitization of vasoconstrictive receptors by G protein-coupled receptor kinases",
abstract = "Liver cirrhosis is complicated by a hyperdynamic circulation characterized by a generalized arterial vasodilatation. This vasodilatation occurs despite high plasma concentration of several potent vasoconstrictive substances like angiotensin, vasopressin, endothelin and norepinephrine. The experimental evidence available shows that compensatory adrenergic and vasoconstrictive signals are not normally transmitted intracellularly. G protein-coupled receptor kinases phosporylate plasma membrane receptors and block the transmission of the signal intracellularly. We hypothesize that these kinases are responsible for the desensitization to vasoconstrictors observed in patients with liver cirrhosis. Pharmacological intervention at this level might be beneficial to treat complications like ascites and variceal bleeding.",
keywords = "Animals, Humans, Hypertension, Portal, Liver, Liver Cirrhosis, Models, Biological, Pressoreceptors, Protein-Serine-Threonine Kinases, Receptors, G-Protein-Coupled, Splanchnic Circulation, Vasoconstriction",
author = "Yogesh Vashist and David Semela and Jean-Fran{\c c}ois Dufour",
year = "2004",
language = "English",
volume = "62",
pages = "82--5",
journal = "MED HYPOTHESES",
issn = "0306-9877",
publisher = "Churchill Livingstone",
number = "1",

}

RIS

TY - JOUR

T1 - Hyperdynamic circulation in liver cirrhosis

T2 - desensitization of vasoconstrictive receptors by G protein-coupled receptor kinases

AU - Vashist, Yogesh

AU - Semela, David

AU - Dufour, Jean-François

PY - 2004

Y1 - 2004

N2 - Liver cirrhosis is complicated by a hyperdynamic circulation characterized by a generalized arterial vasodilatation. This vasodilatation occurs despite high plasma concentration of several potent vasoconstrictive substances like angiotensin, vasopressin, endothelin and norepinephrine. The experimental evidence available shows that compensatory adrenergic and vasoconstrictive signals are not normally transmitted intracellularly. G protein-coupled receptor kinases phosporylate plasma membrane receptors and block the transmission of the signal intracellularly. We hypothesize that these kinases are responsible for the desensitization to vasoconstrictors observed in patients with liver cirrhosis. Pharmacological intervention at this level might be beneficial to treat complications like ascites and variceal bleeding.

AB - Liver cirrhosis is complicated by a hyperdynamic circulation characterized by a generalized arterial vasodilatation. This vasodilatation occurs despite high plasma concentration of several potent vasoconstrictive substances like angiotensin, vasopressin, endothelin and norepinephrine. The experimental evidence available shows that compensatory adrenergic and vasoconstrictive signals are not normally transmitted intracellularly. G protein-coupled receptor kinases phosporylate plasma membrane receptors and block the transmission of the signal intracellularly. We hypothesize that these kinases are responsible for the desensitization to vasoconstrictors observed in patients with liver cirrhosis. Pharmacological intervention at this level might be beneficial to treat complications like ascites and variceal bleeding.

KW - Animals

KW - Humans

KW - Hypertension, Portal

KW - Liver

KW - Liver Cirrhosis

KW - Models, Biological

KW - Pressoreceptors

KW - Protein-Serine-Threonine Kinases

KW - Receptors, G-Protein-Coupled

KW - Splanchnic Circulation

KW - Vasoconstriction

M3 - SCORING: Journal article

C2 - 14729009

VL - 62

SP - 82

EP - 85

JO - MED HYPOTHESES

JF - MED HYPOTHESES

SN - 0306-9877

IS - 1

ER -