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Physiology of Endothelin and the Kidney

  1. Donald E. Kohan1,
  2. Edward W. Inscho2,
  3. Donald Wesson3,
  4. David M. Pollock2

Published Online: 1 APR 2011

DOI: 10.1002/cphy.c100039

Comprehensive Physiology

Comprehensive Physiology

How to Cite

Kohan, D. E., Inscho, E. W., Wesson, D. and Pollock, D. M. 2011. Physiology of Endothelin and the Kidney. Comprehensive Physiology. 1:883–919.

Author Information

  1. 1

    Division of Nephrology, University of Utah Health Sciences Center, and the Salt Lake VA Medical Center, Salt Lake City, Utah

  2. 2

    Vascular Biology Center, Medical College of Georgia, Augusta, Georgia

  3. 3

    Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas

Publication History

  1. Published Online: 1 APR 2011


Since its discovery in 1988 as an endothelial cell-derived peptide that exerts the most potent vasoconstriction of any known endogenous compound, endothelin (ET) has emerged as an important regulator of renal physiology and pathophysiology. This review focuses on how the ET system impacts renal function in health; it is apparent that ET regulates multiple aspects of kidney function. These include modulation of glomerular filtration rate and renal blood flow, control of renin release, and regulation of transport of sodium, water, protons, and bicarbonate. These effects are exerted through ET interactions with almost every cell type in the kidney, including mesangial cells, podocytes, endothelium, vascular smooth muscle, every section of the nephron, and renal nerves. In addition, while not the subject of the current review, ET can also indirectly affect renal function through modulation of extrarenal systems, including the vasculature, nervous system, adrenal gland, circulating hormones, and the heart. As will become apparent, these pleiotropic effects of ET are of fundamental physiologic importance in the control of renal function in health. In addition, to help put these effects into perspective, we will also discuss, albeit to a relatively limited extent, how alterations in the ET system can contribute to hypertension and kidney disease. © 2011 American Physiological Society. Compr Physiol 1:883-919, 2011.