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September 26, 2018AJP Renal PhysiologyOpen Access

Involvement of complement 3 in the salt-sensitive hypertension by activation of renal renin-angiotensin system in spontaneously hypertensive rats

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Population

Spontaneously hypertensive rats (SHR), C3 knockout (KO) SHR, and Wistar-Kyoto (WKY) rats

Comparison

C3 gene knockout via zinc-finger nuclease… vs Wild-type spontaneously hypertensive rats and…

Design

Preclinical

Authors

ENEriko NegishiNFNoboru FukudaUniversity of PittsburghTOTomoyasu OtsukiNihon University

Discussion

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Overview

C3 deletion abolishes salt-sensitive hypertension in rats; hypothesis-generating for complement-targeted approaches but should not yet alter clinical practice.

Structured PICO

P
Population
Spontaneously hypertensive rats (SHR), C3 knockout (KO) SHR, and Wistar-Kyoto (WKY) rats
I
Intervention
C3 gene knockout via zinc-finger nuclease (ZFN) gene-editing technology
C
Comparator
Wild-type spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats
O
Outcome
Blood pressure (salt-sensitive hypertension)surrogate

Complement 3 plays a crucial role in salt-sensitive hypertension by activating the renal renin-angiotensin system and increasing catecholamine excretion in spontaneously hypertensive rats.

Cite This Study

Negishi et al. (2018) studied this question.

synapsesocial.com/papers/6a7e80004c6fed0e030befcfhttps://doi.org/10.1152/ajprenal.00370.2018
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