Endothelins are a family of peptide mediators that have a number of biologi
cal properties. including the ability to act as bronchoconstrictors and vas
oconstrictors of isolated airways and vessels. Endothelin-1 (ET-1) is the m
ore potent peptide compared with the other two peptides of the family.
To examine a possible involvement of ET-1 in the pathogenesis of asthma, we
measured arterial ET-1 levels in 1 1 patients with atopic asthma during at
tack and during remission, and in 11 healthy control subjects. We also perf
ormed fiberoptic bonchoscopy and bronchoalveolar lavage (BAL) to measure ET
-1 levels in the 11 asthmatic patients during remission, and in the 11 heal
thy control subjects. ET-I concentrations in arterial blood and in BAL were
measured by a radioimmunoassay method.
Arterial ET-1 levels were very significantly higher in asthma attack (3.67
+/- 0.51 pg ml(-1)) and in asthma remission (2.65 +/- 10.62 pg ml(-1)) comp
ared with those of the healthy controls (1.37 +/- 0.14 pg ml(-1)) (P<0.001)
. Arterial ET-1 levels were also very significantly higher during asthma at
tack compared with those in asthma remission (P < 0.001). BAL ET-1 levels w
ere significantly higher in asthma remission (0.73 +/- 0.53 pmol g(-1)) com
pared with those of the healthy controls (0.16 +/- 0.02 pmol g(-1)) (Pe 0.0
5). No correlation was observed between arterial and BAL ET-1 levels, Pa-O2
and peak expiratory flow rate (PEFR).
These data are consistent with the hypothesis that ET-1 contributes to the
pathophysiology of asthma. However, it is likely that the true importance o
f this vasoconstrictor peptide will only be revealed by pharmacological stu
dies with specific receptor antagonists.