Volume 70, Issue 10, Pages 1678-1679 (November 2006) Adiponectin versus angiotensin II: Key pathological role of their misbalance  H. Suzuki, S. Eguchi  Kidney International  Volume 70, Issue 10, Pages 1678-1679 (November 2006) DOI: 10.1038/sj.ki.5001936 Copyright © 2006 International Society of Nephrology Terms and Conditions

Figure 1 Pathophysiological signal-transduction interplay between adiponectin and angiotensin II. Peroxisome proliferator-activated receptor-γ (PPARγ) stimulates adiponectin transcription in adipocytes, whereas angiotensin II (Ang II) inhibits it through a reactive oxygen species (ROS)-dependent mechanism. Ang II type-1 (AT1) receptor blocker (ARB) stimulates adiponectin transcription by blocking Ang II binding to the AT1 receptor. Some ARBs directly stimulate PPARγ or may inhibit ROS as antioxidants (pleiotropic actions of ARBs). In the presence of an ARB, Ang II binds to the AT2 receptor. AT2 receptor activation stimulates PPARγ, leading to adiponectin production. In endothelial cells, adiponectin stimulates AMP-activated protein kinase (AMPK) to activate endothelial nitric oxide synthase (eNOS), resulting in nitric oxide (NO) production. This will antagonize Ang II-induced endothelial dysfunction. In vascular smooth muscle cells, adiponectin probably stimulates AMPK, which in turn inhibits extracellular signal-regulated kinase (ERK) activated through epidermal growth factor receptor (EGFR) transactivation by Ang II. This will prevent vascular remodeling induced by Ang II. PPRE, PPAR-responsive element. Kidney International 2006 70, 1678-1679DOI: (10.1038/sj.ki.5001936) Copyright © 2006 International Society of Nephrology Terms and Conditions