Cellular and Genetic Causes of Idiopathic Hyperaldosteronism.

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作者： Kei,Omata ^[1] ; Fumitoshi,Satoh ^[2] ; Ryo,Morimoto ^[3] ; Sadayoshi,Ito ^[2] ; Yuto,Yamazaki ^[3] ; Yasuhiro,Nakamura ^[2] ; Sharath K,Anand ^[2] ; Zeng,Guo ^[4] ; Michael,Stowasser ^[4] ; Hironobu,Sasano ^[5] ; Scott A,Tomlins ^[1] ; William E,Rainey ^[6]

作者单位： From the Department of Pathology (K.O., S.K.A., S.A.T.), University of Michigan, Ann Arbor. ^[1] Division of Nephrology, Endocrinology and Vascular Medicine (K.O., F.S., R.M., S.I.), Tohoku University, Miyagi, Japan. ^[2] Division of Clinical Hypertension, Endocrinology and Metabolism (K.O., F.S.), Tohoku University, Miyagi, Japan. ^[3] Department of Pathology (Y.Y., Y.N., H.S.), Tohoku University, Miyagi, Japan. ^[4] Division of Pathology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Miyagi, Japan (Y.N.). ^[5] Endocrine Hypertension Research Centre, University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals, Brisbane, Australia (Z.G., M.S.). ^[6] Michigan Center for Translational Pathology (S.A.T.), Department of Urology (S.A.T.), Comprehensive Cancer Center (S.A.T.), University of Michigan, Ann Arbor. ^[7] Department of Molecular and Integrative Physiology (W.E.R.), and Department of Medicine (W.E.R.), University of Michigan, Ann Arbor. ^[8]

关键词 adrenal cortex aldosterone calcium channels hyperaldosteronism hypertension