Abstract
Recent studies have provided compelling evidence that tissue kallikrein exerts kinin-independent effects on several renal transporters including the epithelial Na⁺ channel (ENaC), the epithelial calcium channel TRPV5 (transient receptor potential channel vanilloid subtype 5), and the colonic H⁺,K⁺-ATPase. This review focuses on the role of tissue kallikrein in the regulation of renal sodium and potassium handling. Tissue kallikrein is a serine protease involved in the generation of kinins in many organs including the kidney, and most of the renal tissue kallikrein function involves its ability to generate kinins. Tissue kallikrein, through its catalytic activity, acts directly on ENaC in order to modulate its activity but is not critical for the regulation of renal sodium homeostasis. Tissue kallikrein deficient mice exhibit net transepithelial K⁺ absorption in cortical collecting ducts because of abnormal activation of the colonic H⁺,K⁺-ATPase in intercalated cells and reduced K⁺ secretion by principal cells secondary to decreased ENaC activity. Tissue kallikrein is a kaliuretic factor that provides a rapid and aldosterone-independent protection against hyperkalemia after a dietary K⁺load. Tissue kallikrein produced by connecting tubule cells regulates apical transporters by acting from the tubular lumen. Studies have demonstrated the existence of autocrine/paracrine regulatory mechanisms of K⁺ transport in the distal nephron.
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