Secretion of endothelin‐1 and endothelin‐3 by human cultured vascular smooth muscle cells

Yu, Julie C.M.; Davenport, Anthony P.

doi:10.1111/j.1476-5381.1995.tb13262.x

Cited by 67 publications

(46 citation statements)

References 34 publications

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“…However, in some vascular tissues, contractile ETB receptors localized in smooth muscle cells have been described (Moreland et al, 1992;Sumner et al, 1992). has been reported to be secreted by human umbilical vein endothelial cells (Haegerstrand et al, 1989;Hems6n et al, 1991) as well as by vascular smooth muscle cells (Yu & Davenport, 1995). It has been suggested that ET-1 may be involved in the regulation of vascular tone in the foetomaternal region during pregnancy since it has been found to increase to high levels in plasma during delivery (Nisell et al, 1990).…”

Section: Introduction Methodsmentioning

confidence: 99%

Characterization of endothelin receptors in the human umbilical artery and vein

Bogoni

Rizzi

Calò

et al. 1996

British J Pharmacology

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1The aim of the present study was to characterize pharmacologically endothelin receptors that are present in human umbilical vessels. 2 Endothelin-1 (ET-1) and endothelin-2 (ET-2) are potent stimulants of both the human umbilical artery (pEC5o 7.9 and 7.5) and vein (pEC50 8.1 and 8.0). Endothelin-3 (ET-3) is inactive on the artery but contracts the vein (pEC50 7.6). IRL1620 is inactive in both vessels. The order of potency of agonists is suggestive of a typical ETA receptor in the artery (ET-1 = ET-2 > > ET-3) and a mixture of ETA and ETB receptors in the vein (ET-1 = ET-2> ET-3). 3 The selective ETA receptor antagonist, BQ123, competitively inhibits the effect of ET-1 in the human umbilical artery (pA2 6.9), while in the vein, only a mixture of BQ123 and BQ788 (a selective ETB antagonist) weakly displaces to the right the cumulative concentration-response curve to ET-1. Contractions induced by ET-3 in the vein are inhibited by BQ788 (pA2 7.6), but not by BQ123.4 Inhibition of Ca21 channels by nifedipine (0.1 ,uM) is accompanied by a significant decrease of the maximal response to ET-1 by 40% in the artery and by 30% in the vein. The response of the vein to ET-3 is almost abolished by nifedipine. 5 The results indicate that: (i) endothelins contract the human isolated umbilical artery via stimulation of an ETA receptor type; (ii) the contraction induced by ET-1 in the vein is mediated by both ETA and ETB receptors, while ET-3 stimulates the ETB receptor; (iii) the contribution of Ca21 channels to the contraction mediated by the ETB receptor appears to be more important than to that mediated by the ETA receptor.

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Section: Introduction Methodsmentioning

confidence: 99%

Characterization of endothelin receptors in the human umbilical artery and vein

Bogoni

Rizzi

Calò

et al. 1996

British J Pharmacology

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“…In angioplasty-induced neointima in rats, expressions of the mRNAs of endothelin-1, endothelin-3, ECE-1, ETA and ETB receptor were found to be increased (234). Cultured vascular smooth muscle cells explanted from human coronary artery were shown to secrete considerable amounts of endothelin-1 and big endothelin-1 (235). These results are highly suggestive that endothelin-1 may be involved in the development of restenosis following vascular angioplasty, particularly in the case of percutaneous transluminal coronary angioplasty (PTCA).…”

Section: V-5 Vascular Thickeningmentioning

confidence: 99%

Molecular Pharmacology and Pathophysiological Significance of Endothelin

Goto

Hama

Kasuya

1996

Japanese Journal of Pharmacology

159

108

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ABSTRACT-Since the discovery of the most potent vasoconstrictor peptide, endothelin, in 1988, explosive investigations have rapidly clarified much of the basic pharmacological, biochemical and molecular biological features of endothelin, including the presence and structure of isopeptides and their genes (endothelin-1, -2 and -3), regulation of gene expression, intracellular processing, specific endothelia converting enzyme (ECE), receptor subtypes (ETA and ETB), intracellular signal transduction following receptor activation, etc. ECE was recently cloned, and its structure was shown to be a single transmembrane protein with a short intracellular N-terminal and a long extracellular C-terminal that contains the catalytic domain and numerous N-glycosylation sites. In addition to acute contractile or secretory actions, endothelin has been shown to exert long-term proliferative actions on many cell types. In this case, intracellular signal transduction appears to converge to activation of mitogen-activated protein kinase. As a recent dramatic advance, a number of non-peptide and orally active receptor antagonists have been developed. They, as well as current peptide antagonists, markedly accelerated the pace of investigations into the true pathophysiological roles of endogenous endothelin-1 in mature animals; e.g., hypertension, pulmonary hypertension, acute renal failure, cerebral vasospasm, vascular thickening, cardiac hypertrophy, chronic heart failure, etc. Thus, the interference with the endothelin pathway by either ECE-inhibition or receptor blockade may

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“…Smooth muscle cell cultures were obtained as previously de-scribed (Yu & Davenport, 1995 (Chomczynski & Sacchi, 1987). Reverse transcription coupled with polymerase chain reaction was carried out as previously described (O'Reilly et al, 1992;Davenport et al, 1993).…”

Section: Cell Culturementioning

confidence: 99%