Modulation of airway remodeling-associated mediators by the antifibrotic compound, pirfenidone, and the matrix metalloproteinase inhibitor, batimastat, during acute lung injury in mice

Vasopressin (Arg(8)]vasopressin)-induced contraction was characterized using receptor agonists and antagonists for vasopressin and channel blockers in the rat basilar artery ring preparations. Vasopressin induced rhythmic contractions superimposed on a contraction in endothelium-intact preparations but not in denuded ones. Endothelium removal shifted the concentration-response curve for vasopressin leftward and upward. In endothelium-denuded preparations, vasopressin V(1) receptor antagonist shifted the concentration-response curve for vasopressin downward and rightward. Vasopressin V(1) receptor agonist caused contraction but V(2) receptor agonist did not. The contractile response to vasopressin was partly inhibited by nifedipine, SK&F 96365 (1-beta-3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole) and niflumic acid. In the absence of extracellular Ca(2+), vasopressin produced a transient contraction. Charybdotoxin produced an upward and leftward shift of the concentration-response curve for vasopressin. These results suggest that vasopressin elicits contraction due to Ca(2+) influx through voltage-dependent and receptor-operated Ca(2+) channels and to Ca(2+) release from Ca(2+) stores by activating vasopressin V(1) receptors in the rat basilar artery.