Inhibition of dihydropyridine-sensitive calcium entry in hypoxic relaxation of airway smooth muscle.
Am J Physiol
; 268(2 Pt 1): L201-6, 1995 Feb.
Article
in En
| MEDLINE
| ID: mdl-7532368
ABSTRACT
Hypoxia dilates airways in vivo and reduces active tension of airway smooth muscle in vitro. To determine whether hypoxia impairs Ca2+ entry through voltage-dependent channels (VDC), we tested the ability of dihydropyridines to modulate hypoxia-induced relaxation of KCl- and carbamyl choline (carbachol)-contracted porcine bronchi. Carbachol- or KCl-contracted bronchial rings were exposed to progressive hypoxia in the presence or absence of 1 microM BAY K 8644 (an L-type-channel agonist). In separate experiments, rings were contracted with carbachol or KCl, treated with nifedipine (a VDC antagonist), and finally exposed to hypoxia. BAY K 8644 prevented hypoxia-induced relaxation in KCl-contracted bronchi. Nifedipine (10(-5) M) totally relaxed KCl- contracted bronchi. Carbachol-contracted bronchi were only partially relaxed by nifedipine but were completely relaxed when the O2 concentration of the gas was reduced from 95 to 0%. These data indicate that hypoxia can reduce airway smooth muscle tone by limiting entry of Ca2+ through a dihydropyridine-sensitive pathway, but that other mechanisms also contribute to hypoxia-induced relaxation of carbachol-contracted bronchi.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Bronchi
/
Dihydropyridines
/
Calcium
/
Hypoxia
/
Muscle Relaxation
/
Muscle, Smooth
Type of study:
Diagnostic_studies
Limits:
Animals
Language:
En
Journal:
Am J Physiol
Year:
1995
Document type:
Article