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Endothelin-1-induced bronchoconstriction in asthma

G W Chalmers¹, S A Little, K R Patel

¹Department of Respiratory Medicine, West Glasgow Hospitals University NHS Trust, United Kingdom.

American Journal of Respiratory and Critical Care Medicine

|August 1, 1997

Summary

Endothelin-1 (ET-1) causes rapid bronchoconstriction in asthma patients, demonstrating significantly higher potency than methacholine. This study confirms ET-1

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Area of Science:

Pulmonary Medicine
Respiratory Physiology
Pharmacology

Background:

Endothelin-1 (ET-1) is implicated in asthma pathophysiology.
ET-1 is a known potent bronchoconstrictor in vitro and in animal models.

Purpose of the Study:

To compare the effects of inhaled ET-1 and methacholine on airway tone in asthmatics and healthy volunteers.
To assess the safety and potency of inhaled ET-1 in human subjects.

Main Methods:

Double-blind, randomized study involving eight asthmatics and five healthy volunteers.
Inhaled ET-1 and methacholine challenges administered via a dosimeter.
Lung function measured using body plethysmography; endpoints included a 35% fall in specific airway conductance (SGaw) and a 15% fall in FEV1.

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Main Results:

Asthmatics exhibited rapid, dose-dependent bronchoconstriction to ET-1 (mean PC35SGaw: 5.15 nmol), significantly more potent than methacholine (mean PC35SGaw: 0.42 mumol).
Healthy volunteers showed no significant bronchoconstriction to ET-1.
Albuterol rapidly reversed ET-1-induced bronchoconstriction in asthmatics.

Conclusions:

Inhaled Endothelin-1 is a potent bronchoconstrictor in asthma, approximately 100 times more potent than methacholine.
Asthmatics display bronchial hyperreactivity to ET-1.
Nebulized ET-1 (0.96–15.36 nmol) can be safely administered to both asthmatics and healthy individuals.