title: Collecting duct principal cell transport processes and their regulation.
abstract: The principal cell of the kidney collecting duct is one of the most highly regulated epithelial cell types in vertebrates. The effects of hormonal, autocrine, and paracrine factors to regulate principal cell transport processes are central to the maintenance of fluid and electrolyte balance in the face of wide variations in food and water intake. In marked contrast with the epithelial cells lining the proximal tubule, the collecting duct is electrically tight, and ion and osmotic gradients can be very high. The central role of principal cells in salt and water transport is reflected by their defining transporters-the epithelial Na(+) channel (ENaC), the renal outer medullary K(+) channel, and the aquaporin 2 (AQP2) water channel. The coordinated regulation of ENaC by aldosterone, and AQP2 by arginine vasopressin (AVP) in principal cells is essential for the control of plasma Na(+) and K(+) concentrations, extracellular fluid volume, and BP. In addition to these essential hormones, additional neuronal, physical, and chemical factors influence Na(+), K(+), and water homeostasis. Notably, a variety of secreted paracrine and autocrine agents such as bradykinin, ATP, endothelin, nitric oxide, and prostaglandin E2 counterbalance and limit the natriferic effects of aldosterone and the water-retaining effects of AVP. Considerable recent progress has improved our understanding of the transporters, receptors, second messengers, and signaling events that mediate principal cell responses to changing environments in health and disease. This review primarily addresses the structure and function of the key transporters and the complex interplay of regulatory factors that modulate principal cell ion and water transport.
authors.affiliation: Division of Nephrology, Department of Medicine, University of California, San Francisco, California; dpearce@medsfgh.ucsf.edu.
authors.forename: David
authors.initials: D
authors.lastname: Pearce
authors.affiliation: Department of Translational Molecular Pathology, MD Anderson Cancer Center, Houston, Texas;
authors.forename: Rama
authors.initials: R
authors.lastname: Soundararajan
authors.affiliation: Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;
authors.forename: Christiane
authors.initials: C
authors.lastname: Trimpert
authors.affiliation: Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania; and.
authors.forename: Ossama B
authors.initials: OB
authors.lastname: Kashlan
authors.affiliation: Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;
authors.forename: Peter M T
authors.initials: PM
authors.lastname: Deen
authors.affiliation: Division of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah.
authors.forename: Donald E
authors.initials: DE
authors.lastname: Kohan
mesh_terms: D000818:Animals; D051399:Aquaporin 2 / Q000378:metabolism; D001834:Body Water / Q000378:metabolism; D004847:Epithelial Cells / Q000378:metabolism*; D053503:Epithelial Sodium Channels / Q000378:metabolism; D006801:Humans; D017136:Ion Transport; D007685:Kidney Tubules, Collecting / Q000166:cytology / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D015398:Signal Transduction; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014882:Water-Electrolyte Balance
chemical_list: D051399:Aquaporin 2; D053503:Epithelial Sodium Channels; D024661:Potassium Channels, Inwardly Rectifying; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium
keywords: collecting duct; epithelial cell; principal cell; renal physiology