The mechanism of inhibitory effect of AMP kinase for aldosterone-induced vascular damage

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We succeeded in creating vascular-endothelium-specific dominant-negative (dn) and constitutively-active (ca) AMPK transgenic mice using Tet-On expression system. In DOX-treated DOCA-salt TEK-rtTA/TRE-caAMPK mice, endothelium-dependent vasodilatation was significantly ameliorated compared to control DOCA-salt mice. L-NMMA pretreatment to inhibit eNOS completely canceled such ameliorating effect. Endothelium-dependent vasodilatation was significantly attenuated in DOX-treated DOCA-salt TEK-rtTA/TRE-dnAMPK mice thanin control mice. The blood pressure levels of three types DOCA-salt mice (Wt, caAMPK, dnAMPK) were not different, suggesting that such endothelial-protective effect of AMPK was BP-independent.