Endothelin‐1 and endothelin‐3 regulate differently vasoconstrictor responses of smooth muscle of the porcine coronary artery

Ushio‐Fukai, Masuko; Nishimura, Junji; Kobayashi, Sei; Kobayashi, Hideo

doi:10.1111/j.1476-5381.1995.tb14922.x

Cited by 14 publications

(10 citation statements)

References 47 publications

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“…In addition, as demonstrated in Fig. 1B, the maximum contractile response induced by 10 nM ET-1 showed a sustained property similar to those seen in other species (24).…”

Section: Resultssupporting

confidence: 53%

“…In contrast, ET B receptors exist both in the smooth muscle and in the endothelial cells (13,14). While ET B receptors present in the smooth muscle mediate vasoconstriction (13,14,24), those in the endothelial cell cause vasodilation via the release of endothelium-dependent relaxing factors, such as nitric oxide (NO) (12,17,23). However, it has been recently found that part of the depressor effect of ET B receptor may be related to the clearance of ET-1 in the plasma (3,5).…”

mentioning

confidence: 92%

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Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types

Zhou¹,

Dirksen²,

Zweíer³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Mice have been increasingly used as models for investigating cardiovascular diseases. However, the responsiveness of mouse vasculature to endothelin (ET)-1 has not been clearly established. The goal of this study was to determine the role of ET receptors (ET(A) and ET(B)) in mouse vessels using isometric force measurements. Results showed that in the abdominal aorta ET-1 induced a concentration-dependent contraction (EC(50): 1.4 nM) with maximum reaching 89.5 +/- 4.9% (10 nM) of that induced by 60 mM K(+) [with nitric oxide synthase (NOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME)]. However, in the thoracic aorta or the carotid artery, ET-1 was poorly effective. RT-PCR revealed that in the endothelium-denuded abdominal aorta, the PCR product for ET(B) receptors was very low compared with ET(A). Similarly in tissues treated with l-NAME, the ET(B) receptor-specific agonist sarafotoxin 6c (S6c; 100 nM) induced only a minimal contraction (<5%). Meanwhile, the ET(A) antagonist BQ-123 (1 microM) completely inhibited the maximum ET-1 (10 nM) contractile response. Furthermore, we found that in the abdominal aorta that had not been treated with l-NAME, ET-1-induced contraction significantly decreased. However, in such specimens, S6c was unable to induce any relaxation on phenylephrine-induced contraction. These results indicate that the role of ET receptors differs considerably among mouse vessels. In the abdominal aorta, ET(A) receptor mediates a potent vasoconstrictor response, whereas ET(B) has, if any, only a minimal functional presence. Also, our data suggest that ET-1 might involve a NOS-dependent vasodilation in the abdominal aorta, which remains to be further defined.

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“…In addition, as demonstrated in Fig. 1B, the maximum contractile response induced by 10 nM ET-1 showed a sustained property similar to those seen in other species (24).…”

Section: Resultssupporting

confidence: 53%

mentioning

confidence: 92%

Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types

Zhou¹,

Dirksen²,

Zweíer³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…As shown in Figure 1, both ET-1 and ET-3 induced increases in [Ca 2ϩ ] i and tension in a similar concentration range, although the maximal increases in [Ca 2ϩ ] i and tension induced by ET-1 were much greater than those induced by ET-3. This results contrasts with our previous data obtained in the porcine coronary artery (32), in which the concentration range for ET-1-induced tension was much lower than that for ET-3-induced tension. We thus considered that these differences may be due to differences in the distribution of ET-Rs between coronary arterial SMCs and tracheal SMCs, namely, the predominant distribution of ET A -Rs in coronary artery (32) versus a fairly similar distribution of ET A -and ET B -Rs in tracheal SMCs.…”

Section: Discussioncontrasting

confidence: 99%

Expression and Function of Endothelins, Endothelin Receptors, and Endothelin Converting Enzyme in the Porcine Trachea

Yoshimura

Nishimura

Sakihara

et al. 1997

Am J Respir Cell Mol Biol

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Endothelins (ETs) can modulate the airway smooth muscle tone. Using simultaneous measurements of cytosolic Ca2+ concentration ([Ca2+]i) and tension as well as the reverse transcription polymerase chain reaction (RT-PCR), we examined ET systems in the porcine trachea. In the functional study, the application of ET-1, ET-3 or sarafotoxin S6c (S6c) caused increases in [Ca2+]i and tension, in a concentration-dependent manner. These ET ligands were found to increase the Ca2+ sensitivity of the myofilament of the tracheal smooth muscle cells (SMCs). The contractions induced by ET-1 (10(-7) M), an ET receptor (ET-R) non-selective agonist, were much greater than those induced by S6c, an ET(B)-R selective agonist. BQ-123 (10(-6) M), an ET(A)-R antagonist, inhibited the ET-1 induced contraction. These functional experiments suggested the presence of both functioning ET(A)- and ET(B)-Rs in tracheal SMCs. RT-PCR experiments revealed that the tracheal SMCs expressed both ET(A)-R and ET(B)-R mRNAs, while tracheal epithelial cells (EpCs) predominantly expressed ET(A)-R mRNA. The porcine tracheal SMCs and EpCs also expressed pre-pro ET-1 (ppET-1), ppET-3, and endothelin converting enzyme-1 (ECE-1) mRNAs. These results suggested that ETs induce contraction of porcine tracheal SMCs not only by increasing [Ca2+]i but also increasing the Ca2+ sensitivity of the myofilament and that ETs could potentially be the autocrine and/or paracrine transmitters to regulate the contraction in the porcine airway smooth muscle.

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“…If ET does contribute substantially to spasm then these drugs may not be completely effective. Calcium channel antagonists such as nifedipine are only partially effective in blocking vasoconstrictor effects of ET‐1 ( Stork & Cocks, 1994 ) as this agonist mobilizes intracellular calcium stores in addition to stimulating extracellular calcium influx ( Ushio‐Fukai et al ., 1995 ). It has also been suggested that, in vitro , contractions to ET‐1 are not fully reversed by sodium nitroprusside in vein grafts, whereas they are in arterial graft vessels such as mammary artery and gastroepiploic artery ( Uydes‐Dogan et al ., 1996 ).…”

Section: Discussionmentioning

confidence: 99%

Endothelin receptor expression and pharmacology in human saphenous vein graft

Maguire

Davenport

1999

British J Pharmacology

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3 The ratio of medial ET A :ET B receptors was 75% : 25% in both graft and control saphenous vein. 4 ET-1 contracted control (EC 50 2.9 nM) and graft (EC 50 4.5 nM) saphenous vein more potently than diseased coronary artery (EC 50 25.5 nM). 5 In all three blood vessels ET-1 was 100 times more potent than ET-3 and three times more potent than sarafotoxin 6b (S6b). Little or no response was obtained in any vessel with the ET B agonist sarafotoxin 6c (S6c). 6 The ET A antagonist PD156707 (100 nM) blocked ET-1 responses in all three vessels with pK b values of approximately 8.0. 7 For individual graft veins the EC 50 value for ET-1 and`age' of graft in years showed a signi®cant negative correlation. 8 In conclusion there is no alteration in ET receptor expression in the media of saphenous veins grafted into the coronary circulation compared to control veins. ET A receptors predominantly mediate the vasoconstrictor response to ET-1 in graft vein, with no apparent up-regulation of ET B receptors. The sensitivity of the graft vein to ET-1 increased with graft`age', suggesting that these vessels may be particularly vulnerable to the increased plasma ET levels that are detected in patients with cardiovascular disease.

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Endothelin‐1 and endothelin‐3 regulate differently vasoconstrictor responses of smooth muscle of the porcine coronary artery

Cited by 14 publications

References 47 publications

Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types

Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types

Expression and Function of Endothelins, Endothelin Receptors, and Endothelin Converting Enzyme in the Porcine Trachea

Endothelin receptor expression and pharmacology in human saphenous vein graft

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