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Brain-Targeted (Pro) Renin Receptor Knockdown Modulates Body Fluid Homeostasis | OMICS International | Abstract
ISSN: 2167-1095

Journal of Hypertension: Open Access
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Research Article

Brain-Targeted (Pro) Renin Receptor Knockdown Modulates Body Fluid Homeostasis

Theresa Cao1#, Wencheng Li2#, Dale Seth1#, L Gabriel Navar1# and Yumei Feng2*

1Department of Physiology, Tulane University School of Medicine, Tulane Hypertension and Renal Center of Excellence, New Orleans, LA, USA

2Department of Biomedical Sciences, Center for Cardiovascular Research, Colorado State University, Fort Collins, USA

#Authors contributed equally

*Corresponding Author:
Yumei Feng
Department of Biomedical Sciences
Center for Cardiovascular Research
Colorado State University, 1617 Campus Delivery
Fort Collins, CO, 80523
Tel: 970 4913427
E-mail: [email protected]

Received Date: June 05, 2014; Accepted Date: July 17, 2014; Published Date: July 21, 2014

Citation: Cao T, Li W, Seth D, Navar LG, Feng Y (2014) Brain-Targeted (Pro) Renin Receptor Knockdown Modulates Body Fluid Homeostasis. J Hypertens 3:160. doi:10.4172/2167-1095.1000160

Copyright: © 2014 Cao T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Objectives: The (pro) renin receptor (PRR) is highly expressed in the brain and is involved in the central regulation of blood pressure. However, the role of the brain PRR in regulating body fluid homeostasis in hypertension remains unclear. We hypothesized that the brain PRR knockdown modulates water intake, urine, and urinary sodium excretion in the context of angiotensin II (Ang II)-induced hypertension.

Methods and Results: Brain PRR was knocked down in non-transgenic (NT) normotensive and human reninangiotensinogen double-transgenic (RA) mice by intracerebroventricular (ICV) injection of adeno-associated virus expressing short hairpin RNA targeting the PRR (AAV-PRR-shRNA). Water and food intake, and urinary excretion were recorded using metabolic cages. At baseline, RA mice exhibited higher water intake, food intake, urine excretion, urinary sodium excretion and potassium excretion compared to NT mice. PRR knockdown in the brain significantly decreased water and food intake, and urinary potassium and sodium excretion in RA mice, but had no such effects in NT mice. PRR knock down also decreased reactive oxygen species generation and plasma Ang II concentration in RA mice.

Conclusion: PRR knockdown modulates body fluid homeostasis in hypertensive RA mice, suggesting that the brain PRR plays a role in regulating body fluid homeostasis during Ang II-dependent hypertension.


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