Endothelin in the gastrointestinal tract

Takahashi, Kazuhiro; Jones, Philip; Kanse, Sandip M.; Lam, Hing‐Chung; Spokes, R.A.; Ghatei, Mohammad A.; Bloom, Stephen R.

doi:10.1016/0016-5085(90)90472-d

Cited by 117 publications

(24 citation statements)

References 24 publications

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“…In the gastrointestinal tract, the contractile effect of ET on guinea pig ileum [8][9][10], rat stomach and colon [10] has been reported. Recently, we reported that ET had a direct contractile effect on longitudinal smooth muscle cells of guinea pig small intestine [5], On the other hand, Bolger et al [11] reported that ET did not produce any contraction in the guinea pig taenia coli.…”

Section: Discussionmentioning

confidence: 99%

Direct Contractile Effect of Endothelin-1 on Isolated Circular Smooth Muscle Cells of Guinea Pig Caecum

Okabe

Chijiíwa²,

Yoshinaga³

et al. 1995

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Smooth muscle cells isolated from the circular muscle layers of the guinea pig caecum were used to determine whether endothelin-1 (ET-1) can cause contraction by exerting a direct action on smooth muscle cells. In addition, the inhibitory effects of 8-(N, N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), an inhibitor of intracellular Ca²⁺ release, verapamil, a Ca²⁺ channel blocker, and removal of extracellular Ca²⁺ on the ET-1-induced muscle contraction were examined. ET-1 elicited a contractile response of isolated smooth muscle cells in a dose-dependent manner (ED₅₀: 2 nM). TMB-8, verapamil, and removal of extracellular Ca²⁺ significantly inhibited the contraction produced by ET-1. These results strongly suggest that ET-1 has a direct contractile effect on circular smooth muscle cells of the guinea pig caecum, and that this contraction depends on both intracellular and extracellular Ca²⁺.

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Section: Discussionmentioning

confidence: 99%

Direct Contractile Effect of Endothelin-1 on Isolated Circular Smooth Muscle Cells of Guinea Pig Caecum

Okabe

Chijiíwa²,

Yoshinaga³

et al. 1995

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“…These findtract [9]. ET-1 has mainly vasoconstrictive properties by acting on the ET A receptor on smooth muscle cells.…”

Section: Et Plasma Concentration and Hepatic Release In Cirrhosismentioning

confidence: 99%

Endothelin and Other Mediators in the Pathophysiology of Portal Hypertension

Gerbes¹,

Gülberg²,

Bilzer³

1998

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Hyperdynamic circulation as well as increased hepatic resistance contribute to portal hypertension in cirrhosis of the liver [1]. Hyperdynamic circulation with increased cardiac output, heart rate and plasma volume and decreased arterial blood pressure and systemic vasodilatation is pivotal for the hyperdynamic circulation. This has prompted intense research of a number of endogenous neurohumoral mediators with vasodilating properties (NO, natriuretic peptides, glucagon, etc.) [2, 3].

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“…ET was initially isolated from vascular endothelium but could be detected in the gut [2,3], liver [4], kidney [5], lung [6], brain [7] as well as in human plasma [8]. Furthermore, increased ET concentrations in human plasma were found in liver cirrhosis [9][10][11][12][13], acute and Petrowsky/Schmandra/Lorey/Hanisch/ Herrmann chronic renal failure [14,15], congestive heart failure [16], cardiogenic shock [17], and primary hypertension [18].…”

Section: Introductionmentioning

confidence: 99%

Endothelin-Induced Contraction of the Portal Vein in Cirrhosis

et al. 1999

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Endothelin (ET) is one of the most potent vasoconstrictors known so far. It has been proposed that the ET-induced contraction of hepatic stellate cells (Ito, endothelial cells) is an important mechanism for the development of portal hypertension. The purpose of this study was to investigate in an in vitro model whether ET causes a contraction of the portal vein which can contribute to portal hypertension in cirrhosis. Portal veins from normal and cirrhotic rats were used for experiments. Measurements were performed in vitro for cumulative concentrations of ET-1 and ET-3 (1, 5, 10, 50 and 100 nM). Both ETs caused a dose-dependent increase in portal venous tension; the maximal tension (T_max) was measured at 50 nM. The measured T_max was higher for cirrhotic (ET-1: T_max = 189%; ET-3: T_max = 175%) than for normal rats (ET-1: T_max = 130%; ET-3: T_max = 151%). ET-3 produced a higher tension of portal veins in normal rats than ET-1. In conclusion, this study shows that portal veins from cirrhotic rats react more sensitively to ET than those from normal rats. Besides the ET-induced contraction of hepatic stellate cells, contraction of the portal vein and its intrahepatic branches, especially in cirrhotic individuals, has to be considered as a further mechanism of ET contributing to portal hypertension.

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Endothelin in the gastrointestinal tract

Cited by 117 publications

References 24 publications

Direct Contractile Effect of Endothelin-1 on Isolated Circular Smooth Muscle Cells of Guinea Pig Caecum

Direct Contractile Effect of Endothelin-1 on Isolated Circular Smooth Muscle Cells of Guinea Pig Caecum

Endothelin and Other Mediators in the Pathophysiology of Portal Hypertension

Endothelin-Induced Contraction of the Portal Vein in Cirrhosis

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