Long-term portal hypertension increases the vasodilator response to acetylcholine in rat aorta. Role of prostaglandin I2
Résumé
We analyzed both the effect of long-term portal hypertension on the vasomotor response to acetylcholine in rat aorta, and the mechanism involved in this response. For this purpose, sham-operated and prehepatic portal hypertension rats (triple partial portal vein ligation) were used at 21 months after the surgery. The participation of nitric oxide and cyclooxygenase-derivates in the vasodilator response elicited by acetylcholine, after incubation with Nω-nitro-l-arginine methyl ester, indomethacin, SC-560, NS-398, tranylcypromine and furegrelate was analyzed. Nitric oxide, thromboxane B2 and 6-keto prostaglandin F1α releases were measured, and sodium nitroprusside, U-46619, prostaglandin I2 and forskolin vasomotor responses were also analyzed. Cyclooxygenase-1 and cyclooxygenase-2 expression was also analyzed. The acetylcholine vasodilating response was higher in portal hypertensive rats. Thromboxane A2 and nitric oxide release and sodium nitroprusside and U-46619 sensitivity were similar in both groups. Prostaglandin I2 release was not modified by portal hypertension, but vasodilator responses to this prostanoid and to forskolin were higher in portal hypertensive rats. Cyclooxygenase-1 and cyclooxygenase-2 expression remained unmodified by surgery. In conclusion, the increased vasodilation to acetylcholine is maintained in long-term portal hypertension. While the participation of endothelial NO remained unmodified, the COX-2 derivate PGI2 does participate through an increased vasodilator response.
Domaines
Sciences du Vivant [q-bio]
Origine : Fichiers produits par l'(les) auteur(s)
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