Role of Lymphatics in Renal Sodium Handling: Implications for Hypertension

Abstract

Hypertension is the leading risk factor for cardiovascular diseases and strokes [1]. A portion of these patients exhibit SSHTN with high cardiovascular risk and are more difficult to pharmacologically control. The etiology of chronic hypertension includes renal immune cell accumulation and sodium retention. The lymphatic system maintains interstitial homeostasis and an expansion of lymphatic vessels is necessary to resolve inflammation. We have previously demonstrated that ecifically increasing renal lymphatic density prevents HTN in mice [2]. These mice, KidVD+, undergo kidney specific lymphangiogenesis through the overexpression of VEGF-D [3]. The HTN prevention in the KidVD mice is attributed to a common role for lymphatics: a reduction in renal immune cell numbers. We have recently identified that these mice with expanded renal lymphatics demonstrate increased sodium excretion [2]. The aim of this study is to identify the mechanism by which enhancement of renal lymphatics correlates with urinary Na+ excretion, and sensitivity to hypertensive stimuli. To improve the diagnostics and increase treatment efficacy, the mechanism of lymphatic expansion and Na+ retention within the kidney lymphatics may thus prove to be a potential therapeutic target for patients afflicted with SSHTN.