Lymphatic vessels are vital for the trafficking of immune cells from the 
interstitium to draining lymph nodes during inflammation. Hypertension is 
associated with renal infiltration of activated immune cells and inflammation; 
however, it is unknown how renal lymphatic vessels change in hypertension. We 
hypothesized that renal macrophage infiltration and inflammation would cause 
increased lymphatic vessel density in hypertensive rats. Spontaneously 
hypertensive rats (SHR) that exhibit hypertension and renal injury (SHR-A3 
strain) had significantly increased renal lymphatic vessel density and 
macrophages at 40 wk of age compared with Wistar-Kyoto (WKY) controls. SHR rats 
that exhibit hypertension but minimal renal injury (SHR-B2 strain) had 
significantly less renal lymphatic vessel density compared with WKY rats. The 
signals for lymphangiogenesis, VEGF-C and its receptor VEGF-R3, and 
proinflammatory cytokine genes increased significantly in the kidneys of SHR-A3 
rats but not in SHR-B2 rats. Fischer 344 rats exhibit normal blood pressure but 
develop renal injury as they age. Kidneys from 24-mo- and/or 20-mo-old Fischer 
rats had significantly increased lymphatic vessel density, macrophage 
infiltration, VEGF-C and VEGF-R3 expression, and proinflammatory cytokine gene 
expression compared with 4-mo-old controls. These data together demonstrate that 
renal immune cell infiltration and inflammation cause lymphangiogenesis in 
hypertension- and aging-associated renal injury.