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AIM:To examine the participation of HSP90 in portahypertensive rat mesentery in vitro.METHODS:Immunohistochemistry and Western-blot wereused to examine the expression of HSP90 in mesentericvasculature.HSP90 mRNA was detected by RT-PCR,andthe role of HSP90 in hyperdynamic circulation was examinedby in vitro mesenteric perfusion studies.RESULTS:HSP90 was overexpressed in endothelium ofmesentery vasculature in animals with experimental portalhypertension induced by partial portal vein ligation (PVL)compared with normal animals.Geldanamycin (GA),a specialinhibitor of HSP90 signaling,attenuated ACh-dependentvasodilation but did not affect vasodilation in response tosodium nitroprusside in normal rats.In PVL animals,theperfused mesentery was hyporesponsive to vasoconstrictormethoxamine.GA significantly potentiated methoxamine-induced vasoconstrictor after PVL.CONCLUSION:HSP90 plays a key role in NO-dependenthyperdynamic circulation in portal hypertension and providesa novel method for future treatment of portal hypertension.
AIM: To examine the participation of HSP90 in portahypertensive rat mesentery in vitro. METHODS: Immunohistochemistry and Western-blot wereused to examine the expression of HSP90 in mesentericvasculature. HSP90 mRNA was detected by RT-PCR, and the role of HSP90 in hyperdynamic circulation was examinedby in vitro mesenteric perfusion studies .RESULTS: HSP90 was overexpressed in endothelium ofmesentery vasculature in animals with experimental portal hypertypemia induced by partial portal vein ligation (PVL) compared with normal animals.Geldanamycin (GA), a special inhibitor of HSP90 signaling, attenuated ACh-dependentvasodilation but did not affect vasodilation in response tosodium nitroprusside in normal rats. In PVL animals, the perfused mesentery was hyporesponsive to vasoconstrictormethoxamine. GA significantly potentiated methoxamine-induced vasoconstrictor after PVL. CONCLUSION: HSP90 plays a key role in NO-dependent hyperdynamic circulation in portal hypertension and provides novel method for future treatment of portal hypertension.