Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis

N. M. Atucha, Vijay Shah, G. Garcia-Cardena, W. E. Sessa, R. J. Groszmann

Research output: Contribution to journalArticle

73 Citations (Scopus)

Abstract

Background and Aims: Previous studies have shown that nitric oxide synthesis inhibition corrects the hyporesponsiveness to vasoconstrictors present in the mesenteric vascular bed of portal-hypertensive rats. The origin of this elevated NO production, whether endothelial or muscular, is unknown. The aim of this study was to evaluate the role of vascular endothelium in the hyporesponsiveness to methoxamine (MTX) in the mesenteric vascular bed of portal vein-ligated (PVL) and cirrhotic rats. Methods: Endothelial denudation was achieved using a combined treatment of cholic acid and distilled water. Results: Compared with the respective control groups, PVL rats showed a reduced vascular response to MTX. Similar results were obtained in cirrhotic animals. The presence of ascites was associated with a more severe reduction in the response to MTX. Removal of the endothelium completely corrected the vascular hyporesponsiveness of PVL, cirrhotic nonascitic, and ascitic animals. In these experiments, acetylcholine-mediated vasodilation was practically absent whereas that of sodium nitroprusside was potentiated, which indicates a successful elimination of the endothelium and the preservation of smooth muscle function. Immunostaining for NO synthase isoforms revealed the presence of endothelial NO synthase protein in healthy and PVL rats exclusively in the endothelium. Conclusions: The mesenteric vascular hyporesponsiveness to MTX present in these models of liver diseases and portal hypertension is solely due to endothelium-dependent factors.

Original languageEnglish (US)
Pages (from-to)1627-1632
Number of pages6
JournalGastroenterology
Volume111
Issue number6
StatePublished - 1996
Externally publishedYes

Fingerprint

Portal Hypertension
Methoxamine
Liver Cirrhosis
Endothelium
Blood Vessels
Portal Vein
Nitric Oxide Synthase
Cholic Acid
Vascular Endothelium
Nitroprusside
Vasoconstrictor Agents
Ascites
Vasodilation
Acetylcholine
Smooth Muscle
Liver Diseases
Nitric Oxide
Protein Isoforms
Control Groups
Water

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Atucha, N. M., Shah, V., Garcia-Cardena, G., Sessa, W. E., & Groszmann, R. J. (1996). Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis. Gastroenterology, 111(6), 1627-1632.

Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis. / Atucha, N. M.; Shah, Vijay; Garcia-Cardena, G.; Sessa, W. E.; Groszmann, R. J.

In: Gastroenterology, Vol. 111, No. 6, 1996, p. 1627-1632.

Research output: Contribution to journalArticle

Atucha, NM, Shah, V, Garcia-Cardena, G, Sessa, WE & Groszmann, RJ 1996, 'Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis', Gastroenterology, vol. 111, no. 6, pp. 1627-1632.
Atucha, N. M. ; Shah, Vijay ; Garcia-Cardena, G. ; Sessa, W. E. ; Groszmann, R. J. / Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis. In: Gastroenterology. 1996 ; Vol. 111, No. 6. pp. 1627-1632.
@article{17fe693c424148f7813da97c833cbc7e,
title = "Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis",
abstract = "Background and Aims: Previous studies have shown that nitric oxide synthesis inhibition corrects the hyporesponsiveness to vasoconstrictors present in the mesenteric vascular bed of portal-hypertensive rats. The origin of this elevated NO production, whether endothelial or muscular, is unknown. The aim of this study was to evaluate the role of vascular endothelium in the hyporesponsiveness to methoxamine (MTX) in the mesenteric vascular bed of portal vein-ligated (PVL) and cirrhotic rats. Methods: Endothelial denudation was achieved using a combined treatment of cholic acid and distilled water. Results: Compared with the respective control groups, PVL rats showed a reduced vascular response to MTX. Similar results were obtained in cirrhotic animals. The presence of ascites was associated with a more severe reduction in the response to MTX. Removal of the endothelium completely corrected the vascular hyporesponsiveness of PVL, cirrhotic nonascitic, and ascitic animals. In these experiments, acetylcholine-mediated vasodilation was practically absent whereas that of sodium nitroprusside was potentiated, which indicates a successful elimination of the endothelium and the preservation of smooth muscle function. Immunostaining for NO synthase isoforms revealed the presence of endothelial NO synthase protein in healthy and PVL rats exclusively in the endothelium. Conclusions: The mesenteric vascular hyporesponsiveness to MTX present in these models of liver diseases and portal hypertension is solely due to endothelium-dependent factors.",
author = "Atucha, {N. M.} and Vijay Shah and G. Garcia-Cardena and Sessa, {W. E.} and Groszmann, {R. J.}",
year = "1996",
language = "English (US)",
volume = "111",
pages = "1627--1632",
journal = "Gastroenterology",
issn = "0016-5085",
publisher = "W.B. Saunders Ltd",
number = "6",

}

TY - JOUR

T1 - Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis

AU - Atucha, N. M.

AU - Shah, Vijay

AU - Garcia-Cardena, G.

AU - Sessa, W. E.

AU - Groszmann, R. J.

PY - 1996

Y1 - 1996

N2 - Background and Aims: Previous studies have shown that nitric oxide synthesis inhibition corrects the hyporesponsiveness to vasoconstrictors present in the mesenteric vascular bed of portal-hypertensive rats. The origin of this elevated NO production, whether endothelial or muscular, is unknown. The aim of this study was to evaluate the role of vascular endothelium in the hyporesponsiveness to methoxamine (MTX) in the mesenteric vascular bed of portal vein-ligated (PVL) and cirrhotic rats. Methods: Endothelial denudation was achieved using a combined treatment of cholic acid and distilled water. Results: Compared with the respective control groups, PVL rats showed a reduced vascular response to MTX. Similar results were obtained in cirrhotic animals. The presence of ascites was associated with a more severe reduction in the response to MTX. Removal of the endothelium completely corrected the vascular hyporesponsiveness of PVL, cirrhotic nonascitic, and ascitic animals. In these experiments, acetylcholine-mediated vasodilation was practically absent whereas that of sodium nitroprusside was potentiated, which indicates a successful elimination of the endothelium and the preservation of smooth muscle function. Immunostaining for NO synthase isoforms revealed the presence of endothelial NO synthase protein in healthy and PVL rats exclusively in the endothelium. Conclusions: The mesenteric vascular hyporesponsiveness to MTX present in these models of liver diseases and portal hypertension is solely due to endothelium-dependent factors.

AB - Background and Aims: Previous studies have shown that nitric oxide synthesis inhibition corrects the hyporesponsiveness to vasoconstrictors present in the mesenteric vascular bed of portal-hypertensive rats. The origin of this elevated NO production, whether endothelial or muscular, is unknown. The aim of this study was to evaluate the role of vascular endothelium in the hyporesponsiveness to methoxamine (MTX) in the mesenteric vascular bed of portal vein-ligated (PVL) and cirrhotic rats. Methods: Endothelial denudation was achieved using a combined treatment of cholic acid and distilled water. Results: Compared with the respective control groups, PVL rats showed a reduced vascular response to MTX. Similar results were obtained in cirrhotic animals. The presence of ascites was associated with a more severe reduction in the response to MTX. Removal of the endothelium completely corrected the vascular hyporesponsiveness of PVL, cirrhotic nonascitic, and ascitic animals. In these experiments, acetylcholine-mediated vasodilation was practically absent whereas that of sodium nitroprusside was potentiated, which indicates a successful elimination of the endothelium and the preservation of smooth muscle function. Immunostaining for NO synthase isoforms revealed the presence of endothelial NO synthase protein in healthy and PVL rats exclusively in the endothelium. Conclusions: The mesenteric vascular hyporesponsiveness to MTX present in these models of liver diseases and portal hypertension is solely due to endothelium-dependent factors.

UR - http://www.scopus.com/inward/record.url?scp=0029846461&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029846461&partnerID=8YFLogxK

M3 - Article

VL - 111

SP - 1627

EP - 1632

JO - Gastroenterology

JF - Gastroenterology

SN - 0016-5085

IS - 6

ER -