Endothelin (ET)-1 induced mucosal damage in the rat small intestine

Role of ETA receptors

Steffen Massberg, M. Borós, Rosmarie Leiderer, Lajos Baranyi, Hidechika Okada, Konrad Messmer

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

The role of endothelin (ET)-1 as a mediator of small intestinal mucosal perfusion failure and tissue damage was investigated in the rat using intravital fluorescence videomicroscopy. The effects of intravenous infusion of ET-1 (3 nmol/kg) on functional capillary density, mucosal thickness, and the degree of mucosal damage were evaluated. Administration of ET-1 caused pronounced mucosal injury with a significant reduction of mucosal thickness compared with vehicle-treated control animals. Concomitantly, villous functional capillary density was markedly reduced 30 and 90 min after the infusion of ET-1. ETA receptor blockade by pretreatment with BQ 610 or with the novel ETA receptor antagonist ETR-P1/FL peptide prevented ET-1 induced capillary perfusion failure and mucosal damage. In contrast, the ETB receptor antagonist IRL 1038 was not effective. These results indicate that, acting via the ETA receptor, elevated levels of circulating ET-1 under various pathophysiological conditions, such as septic or hemorrhagic shock, might impair nutritive perfusion of the intestinal mucosa and contribute to tissue injury.

Original languageEnglish
Pages (from-to)177-183
Number of pages7
JournalShock
Volume9
Issue number3
Publication statusPublished - Mar 1998

Fingerprint

Endothelin-1
Small Intestine
Perfusion
Endothelin-3
Video Microscopy
Hemorrhagic Shock
Wounds and Injuries
Intestinal Mucosa
Septic Shock
Intravenous Infusions
Fluorescence
Peptides

ASJC Scopus subject areas

  • Physiology
  • Critical Care and Intensive Care Medicine

Cite this

Massberg, S., Borós, M., Leiderer, R., Baranyi, L., Okada, H., & Messmer, K. (1998). Endothelin (ET)-1 induced mucosal damage in the rat small intestine: Role of ETA receptors. Shock, 9(3), 177-183.

Endothelin (ET)-1 induced mucosal damage in the rat small intestine : Role of ETA receptors. / Massberg, Steffen; Borós, M.; Leiderer, Rosmarie; Baranyi, Lajos; Okada, Hidechika; Messmer, Konrad.

In: Shock, Vol. 9, No. 3, 03.1998, p. 177-183.

Research output: Contribution to journalArticle

Massberg, S, Borós, M, Leiderer, R, Baranyi, L, Okada, H & Messmer, K 1998, 'Endothelin (ET)-1 induced mucosal damage in the rat small intestine: Role of ETA receptors', Shock, vol. 9, no. 3, pp. 177-183.
Massberg S, Borós M, Leiderer R, Baranyi L, Okada H, Messmer K. Endothelin (ET)-1 induced mucosal damage in the rat small intestine: Role of ETA receptors. Shock. 1998 Mar;9(3):177-183.
Massberg, Steffen ; Borós, M. ; Leiderer, Rosmarie ; Baranyi, Lajos ; Okada, Hidechika ; Messmer, Konrad. / Endothelin (ET)-1 induced mucosal damage in the rat small intestine : Role of ETA receptors. In: Shock. 1998 ; Vol. 9, No. 3. pp. 177-183.
@article{66025f105a51403e9df74bfe345b6ae6,
title = "Endothelin (ET)-1 induced mucosal damage in the rat small intestine: Role of ETA receptors",
abstract = "The role of endothelin (ET)-1 as a mediator of small intestinal mucosal perfusion failure and tissue damage was investigated in the rat using intravital fluorescence videomicroscopy. The effects of intravenous infusion of ET-1 (3 nmol/kg) on functional capillary density, mucosal thickness, and the degree of mucosal damage were evaluated. Administration of ET-1 caused pronounced mucosal injury with a significant reduction of mucosal thickness compared with vehicle-treated control animals. Concomitantly, villous functional capillary density was markedly reduced 30 and 90 min after the infusion of ET-1. ETA receptor blockade by pretreatment with BQ 610 or with the novel ETA receptor antagonist ETR-P1/FL peptide prevented ET-1 induced capillary perfusion failure and mucosal damage. In contrast, the ETB receptor antagonist IRL 1038 was not effective. These results indicate that, acting via the ETA receptor, elevated levels of circulating ET-1 under various pathophysiological conditions, such as septic or hemorrhagic shock, might impair nutritive perfusion of the intestinal mucosa and contribute to tissue injury.",
author = "Steffen Massberg and M. Bor{\'o}s and Rosmarie Leiderer and Lajos Baranyi and Hidechika Okada and Konrad Messmer",
year = "1998",
month = "3",
language = "English",
volume = "9",
pages = "177--183",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Endothelin (ET)-1 induced mucosal damage in the rat small intestine

T2 - Role of ETA receptors

AU - Massberg, Steffen

AU - Borós, M.

AU - Leiderer, Rosmarie

AU - Baranyi, Lajos

AU - Okada, Hidechika

AU - Messmer, Konrad

PY - 1998/3

Y1 - 1998/3

N2 - The role of endothelin (ET)-1 as a mediator of small intestinal mucosal perfusion failure and tissue damage was investigated in the rat using intravital fluorescence videomicroscopy. The effects of intravenous infusion of ET-1 (3 nmol/kg) on functional capillary density, mucosal thickness, and the degree of mucosal damage were evaluated. Administration of ET-1 caused pronounced mucosal injury with a significant reduction of mucosal thickness compared with vehicle-treated control animals. Concomitantly, villous functional capillary density was markedly reduced 30 and 90 min after the infusion of ET-1. ETA receptor blockade by pretreatment with BQ 610 or with the novel ETA receptor antagonist ETR-P1/FL peptide prevented ET-1 induced capillary perfusion failure and mucosal damage. In contrast, the ETB receptor antagonist IRL 1038 was not effective. These results indicate that, acting via the ETA receptor, elevated levels of circulating ET-1 under various pathophysiological conditions, such as septic or hemorrhagic shock, might impair nutritive perfusion of the intestinal mucosa and contribute to tissue injury.

AB - The role of endothelin (ET)-1 as a mediator of small intestinal mucosal perfusion failure and tissue damage was investigated in the rat using intravital fluorescence videomicroscopy. The effects of intravenous infusion of ET-1 (3 nmol/kg) on functional capillary density, mucosal thickness, and the degree of mucosal damage were evaluated. Administration of ET-1 caused pronounced mucosal injury with a significant reduction of mucosal thickness compared with vehicle-treated control animals. Concomitantly, villous functional capillary density was markedly reduced 30 and 90 min after the infusion of ET-1. ETA receptor blockade by pretreatment with BQ 610 or with the novel ETA receptor antagonist ETR-P1/FL peptide prevented ET-1 induced capillary perfusion failure and mucosal damage. In contrast, the ETB receptor antagonist IRL 1038 was not effective. These results indicate that, acting via the ETA receptor, elevated levels of circulating ET-1 under various pathophysiological conditions, such as septic or hemorrhagic shock, might impair nutritive perfusion of the intestinal mucosa and contribute to tissue injury.

UR - http://www.scopus.com/inward/record.url?scp=0032013150&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032013150&partnerID=8YFLogxK

M3 - Article

VL - 9

SP - 177

EP - 183

JO - Shock

JF - Shock

SN - 1073-2322

IS - 3

ER -