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Vol. 286, Issue 3, 1309-1314, September 1998
Department of Pathology, Prostanoids have been implicated in the regulation of lung vascular
tone both under physiological and inflammatory conditions. The
conversion of arachidonic acid (AA) to prostaglandin H2 is catalyzed at least by two isoforms of cyclooxygenase, named Cox-1 and
Cox-2. Cox-1 is thought to be ubiquitously expressed, enrolled in
physiological processes, whereas Cox-2 is mostly assumed to be
dynamically regulated, responding to inflammatory conditions. We have
recently shown by immunohistochemistry that Cox-2 is constitutively expressed in control rat lungs, with a predominant localization in
smooth muscle cells of partially muscular vessels. We now asked whether
Cox-2 is basically involved in the physiological regulation of
pulmonary vascular tone. Isolated perfused rat lungs were challenged with intravascular bolus application of free AA to elicit
thromboxane-related vasoconstrictor responses and to investigate the
effects of three different selective Cox-2 inhibitors (NS-398, DUP697,
SC-236). AA induced the liberation of prostaglandin I2 and
thromboxane A2 into the intravascular space, and it
provoked marked pulmonary artery pressure responses and concomitant
lung edema formation. All events were dose-dependently inhibited by 1 to 50 µmol/liter NS-398, whereas control vasoconstrictor responses to
angiotensin II and the stable thromboxane analogue U46619 were not
affected by this agent. Similarly, marked inhibition of the AA elicited pressor response was achieved by 25 µmol/l DUP697 and by 10 µmol/l SC-236. These data suggest a physiological role of Cox-2 rather than
Cox-1 in the regulation of vascular tone in rat lungs.
0022-3565/98/2863-1309$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics
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