Hyperosmolarity-induced relaxation and prostaglandin release in guinea pigtrachea in vitro

In this study, a tracheal perfusion apparatus was used to investigate the n ature of the relaxing factor released by hyperosmolarity on the epithelial side of guinea pig trachea. NaCl induced concentration-dependent relaxation . This relaxation was not affected when the trachea was preincubated with a vasoactive intestinal peptide (VIP) receptor antagonist or with the nitric oxide synthesis inhibitor N-G-monomethyl-L-arginine (L-NMMA). When the pro staglandin synthesis was prevented by preincubation with the phospholipase A(2)-inhibitor quinacrine, or the cyclooxygenase inhibitor indomethacin, th e maximal relaxation induced by NaCl was suppressed by 50% (P < 0.05). More over, the prostaglandin E-2 concentration was four times higher (P < 0.05) in the organ bath during the relaxations, whereas the nitric oxide concentr ation remained unchanged. In conclusion, increased osmolarity on the airway surface leads to the release of prostaglandins, which are involved in part in the hyperosmolarity-induced relaxation of airway smooth muscle. This mi ght be relevant for asthmatic patients since prostaglandin may modulate the bronchoconstrictive response to hyperosmolar stimuli and exercise. (C) 200 0 Elsevier Science B.V. All rights reserved.