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INVITED REVIEW

Regulation of cation transport in the distal nephron by mechanical forces

¹Division of Pediatric Nephrology, Department of Pediatrics, Mount Sinai School of Medicine, New York, New York; and ²Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania

Submitted 30 May 2006 ; accepted in final form 12 July 2006

Thiazide and loop diuretics induce renal K⁺ secretion, often leading to renal K⁺ wasting and hypokalemia. This phenomenon has been proposed to reflect an increase in delivery to and reabsorption of Na⁺ by the distal nephron, with a resultant increase in the driving force for passive K⁺ efflux across the apical membrane. Recent studies suggest that cellular mechanisms that lead to enhanced rates of Na⁺ reabsorption as well as K⁺ secretion in response to increases tubular flow rates are more complex. Increases in tubular flow rates directly enhance the activity of apical membrane Na⁺ channels and indirectly activate a class of K⁺ channels, referred to as maxi-K, that are functionally inactive under low flow states. This review addresses the role of biomechanical forces, generated by variations in urinary flow rate and tubular fluid volume, in the regulation of transepithelial Na⁺ and K⁺ transport in the distal nephron. The question of why the distal nephron has evolved to include a component of flow-dependent K⁺ secretion is also addressed.

epithelial Na⁺ channel; ROMK; cortical collecting duct; shear stress; SK channel

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