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Departments of 1 Pharmacology and 2 Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198
Received 8 July 1996; accepted in final form 17 June 1997.
Toews, M. L., E. E. Ustinova, and H. D. Schultz.
Lysophosphatidic acid enhances contractility of isolated airway
smooth muscle. J. Appl. Physiol.
83(4): 1216-1222, 1997.
The effects of the simple phospholipid
mediator lysophosphatidic acid (LPA) on the contractile responsiveness
of isolated tracheal rings from rabbits and cats were assessed. In both
species, LPA increased the contractile response to the muscarinic
agonist methacholine, but LPA did not induce contraction on its own.
Conversely, LPA decreased the relaxation response to the
-adrenergic-agonist isoproterenol in both species. Concentrations of
LPA as low as 10
8 M were
effective, and the effects of LPA were rapidly reversed on washing.
Phosphatidic acid was much less effective, requiring higher
concentrations and producing only a minimal effect. Contractions induced by serotonin and by substance P also were enhanced by LPA, but
KCl-induced contractions were unaffected. LPA inhibited the
isoproterenol-induced relaxation of KCl-precontracted rings, similar to
its effects on methacholine-precontracted rings, and relaxation induced
by the direct adenylyl cyclase activator forskolin was inhibited in a
manner similar to that induced by isoproterenol. Epithelium removal did
not alter the contraction-enhancing effect of LPA. The ability of LPA
to both enhance contraction and inhibit relaxation of airway smooth
muscle suggests that LPA could contribute to airway hypercontractility
in asthma, airway inflammation, or other types of lung injury.
bronchoconstriction
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