Journal
PHARMACEUTICS
Volume 14, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/pharmaceutics14010084
Keywords
kidney; lymphatics; inflammation; immunity; hypertension
Categories
Funding
- National Institutes of Health [RO1 DK119497, DK120493, RO1 DK120493]
- Texas A&M University Triads for Transformation T3
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Renal lymphangiogenesis can lower blood pressure and is associated with favorable alterations in renal immune cells and increased sodium excretion.
Chronic interstitial inflammation and renal infiltration of activated immune cells play an integral role in hypertension. Lymphatics regulate inflammation through clearance of immune cells and excess interstitial fluid. Previously, we demonstrated increasing renal lymphangiogenesis prevents hypertension in mice. We hypothesized that targeted nanoparticle delivery of vascular endothelial growth factor-C (VEGF-C) to the kidney would induce renal lymphangiogenesis, lowering blood pressure in hypertensive mice. A kidney-targeting nanoparticle was loaded with a VEGF receptor-3-specific form of VEGF-C and injected into mice with angiotensin II-induced hypertension or LNAME-induced hypertension every 3 days. Nanoparticle-treated mice exhibited increased renal lymphatic vessel density and width compared to hypertensive mice injected with VEGF-C alone. Nanoparticle-treated mice exhibited decreased systolic blood pressure, decreased pro-inflammatory renal immune cells, and increased urinary fractional excretion of sodium. Our findings demonstrate that pharmacologically expanding renal lymphatics decreases blood pressure and is associated with favorable alterations in renal immune cells and increased sodium excretion.
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