Involvement of the Endothelins in Airway Reactivity and Disease

Goldie, Roy G.; Henry, Peter J.

doi:10.1007/978-3-642-56899-2_14

Endothelin and Its Inhibitors

2001

DOI: 10.1007/978-3-642-56899-2_14

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Involvement of the Endothelins in Airway Reactivity and Disease

Roy G. Goldie¹,

Peter J. Henry²

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Cited by 2 publications

(1 citation statement)

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“…ET-1 also has pro-inflammatory actions in the airways, stimulating the release of inflammatory cytokines. 3 We have previously shown that respiratory tract viral infection with parainfluenza-1, 4 parainfluenza-3 5 and influenza-A 6 is associated with changes in ET receptor function and distribution in airway smooth muscle. We have also shown that influenza-A virus infection with associated airway inflammation markedly increased ET production in mouse airways.…”

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confidence: 99%

The Impact of Respiratory Syncytial Virus Infection on Endothelin Receptor Function and Release in Sheep Bronchial Explants

Fernandes¹,

D'Aprile²,

Self³

et al. 2004

Journal of Cardiovascular Pharmacology

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We investigated the impact of respiratory syncytial virus (RSV) infection, an important asthma precipitant, on endothelin receptor function and release in sheep bronchial explants. RSV infection was confirmed using polymerase chain reaction and immunohistochemistry. Since sheep airway smooth muscle contains only endothelin-A receptors, sarafotoxin (Stx) S6c did not cause airway contraction. In contrast, sarafotoxin S6c (300 nM) caused contraction in RSV-infected bronchial explants (8 +/- 3% carbachol Emax). However, we could not detect airway smooth muscle endothelin-B receptors in explants using autoradiography. RSV infection per se did not alter the release of immunoreactive endothelin from sheep bronchial explants (control = 11.6 +/- 0.9 pg versus RSV = 12.1 +/- 0.9 pg). Interestingly, dexamethasone (1 microM) alone increased endothelin release in both control (17.9 +/- 2.0 pg) and RSV-infected tissue (18.3 +/- 3.1 pg). The combined presence of protease-activated receptor-2 (PAR-2) ligand (100 microM) and dexamethasone (1 microM) also increased endothelin release from control tissue (17.3 +/- 1.4 pg), but endothelin release was suppressed by PAR-2 ligand in RSV-infected tissue (10.3 +/- 0.8 pg), probably because PAR-2 expression was increased by RSV. In summary, the novel expression of endothelin-B receptors triggered by RSV might be relevant to RSV-associated asthma. Furthermore, activation of airway PAR-2 may be protective in asthma where endothelin levels are elevated in part via endothelin release suppression.

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mentioning

confidence: 99%

The Impact of Respiratory Syncytial Virus Infection on Endothelin Receptor Function and Release in Sheep Bronchial Explants

Fernandes¹,

D'Aprile²,

Self³

et al. 2004

Journal of Cardiovascular Pharmacology

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Dipeptide sulfonamides as endothelin ET_A/ET_B receptor antagonists

Ksander¹,

Shetty²,

DelGrande³

et al. 2002

Can. J. Physiol. Pharmacol.

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We studied the effect of long-term treatment with the oral endothelin (ET) ET A antagonist 2-benzo[1,3]dioxol-5-yl-3-ben-zyl-4-(4-methoxy-phenyl-)-4-oxobut-2-enoate-sodium (PD 155080; PD) on right ventricular intracellular calcium (Ca 2 i) handling and cardiac and pulmonary artery function in control rats and rats with monocrotaline (MCT)-induced right-heart hypertrophy. Rats were given an intraperitoneal injection of either saline (controls; n 9) or MCT (50 mg/kg; n 12), resulting in pulmonary hypertension-induced myocardial hyper-trophy, or MCT followed by the daily administration of PD (50 mg/kg) for 9 weeks (n 9). After 9 weeks, right ventricular pressure was measured, and the hearts were removed and perfused in vitro. Right ventricular function and Ca 2 i transients were recorded simultaneously on a beat-to-beat basis using aequorin. Surviving animals in the MCT group (58%) developed significant hypertrophy and had 2-fold higher right ventricu-lar pressure and a prolonged duration of isovolumic contraction that correlated with a similar prolongation of the Ca 2 i transient, indicating a reduced rate of Ca 2 sequestration in hypertrophy (P 0.05 versus control). In the PD group, all animals survived, and right ventricular pressure, diastolic relaxation, Ca 2 transport kinetics, and peak systolic and end-diastolic wall stress were all normalized (P 0.05 versus control); and pulmonary artery endothelial function was partly restored (P 0.05 versus MCT and control groups). These results demonstrate for the first time that long-term ET A receptor antagonism normalizes myocardial cytosolic Ca 2 modulation, which may contribute to the antihypertro-phic and cardioprotective effect of ET A receptor therapy in this model. The polypeptide endothelin-1 (ET-1) plays an important role in the cardiovascular system by modulating vasomotion, inotropic state, and growth processes. ET-1 exerts its different biological effects via the activation of specific receptors (ET A and ET B receptors) which are widely expressed on cardiac and vascular cells of both humans and other species (Rubanyi and Polokoff, 1994). Cardiac hypertrophy is an adaptational mechanism to stresses such as neurohumoral stimulation and pressure overload (Homcy, 1998). Recent observations suggest the involvement of ET-1 in left ventricular hypertrophy, but much less is known about its role in right ventricular hypertrophy (Ito, 1997; Kirchengast and Mü nter, 1999). In several rat models of right ventricular hypertrophy, including exposure to normobaric hypoxia, carbon monoxide, MCT (Miyauchi et al., 1993), or volume overload (Brown et al., 1995), prepro-ET-1 mRNA transcription was increased in right atria or ventricles without consistent increase in myocardial ET-1 production. In a recent study, we found no evidence for increased release of ET-1 and big ET-1 in hypertrophic hearts and concluded that the growth process may be fueled by extracardiac ET (Brunner, 1999). Administration of ET A antagonists (Miyauchi et al. over several weeks generally attenuated t...

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Involvement of the Endothelins in Airway Reactivity and Disease

Cited by 2 publications

References 213 publications

The Impact of Respiratory Syncytial Virus Infection on Endothelin Receptor Function and Release in Sheep Bronchial Explants

The Impact of Respiratory Syncytial Virus Infection on Endothelin Receptor Function and Release in Sheep Bronchial Explants

Dipeptide sulfonamides as endothelin ET_A/ET_B receptor antagonists

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Involvement of the Endothelins in Airway Reactivity and Disease

Cited by 2 publications

References 213 publications

The Impact of Respiratory Syncytial Virus Infection on Endothelin Receptor Function and Release in Sheep Bronchial Explants

The Impact of Respiratory Syncytial Virus Infection on Endothelin Receptor Function and Release in Sheep Bronchial Explants

Dipeptide sulfonamides as endothelin ETA/ETB receptor antagonists

Contact Info

Product

Resources

About

Dipeptide sulfonamides as endothelin ET_A/ET_B receptor antagonists