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April 23, 2013Journal of Clinical InvestigationOpen Access

The absence of intrarenal ACE protects against hypertension

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Why the study?

Does the absence of kidney ACE blunt hypertension and renal responses induced by Ang II infusion or nitric oxide synthesis inhibition in mice?

Population

Mice specifically lacking kidney angiotensin-converting enzyme (ACE) and wild-type mice

Comparison

Experimental hypertension induced by Ang II… vs Wild-type mice subjected to the same…

Design

Preclinical

Authors

RGRomer A. González-VillalobosJohnson & Johnson (United States)TJTea JanjouliaCedars-Sinai Medical CenterNFNicholas FletcherCornell University

Discussion

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Implication

Kidney ACE may drive experimental hypertension in mice; leaves open human relevance and need for translational studies.

Structured PICO

Does the absence of kidney ACE blunt hypertension and renal responses induced by Ang II infusion or nitric oxide synthesis inhibition in mice?

P
Population
Mice specifically lacking kidney angiotensin-converting enzyme (ACE) and wild-type mice
I
Intervention
Experimental hypertension induced by Ang II infusion or nitric oxide synthesis inhibition
C
Comparator
Wild-type mice subjected to the same experimental hypertension models
O
Outcome
Blood pressure response to experimental hypertensionsurrogate

Renal ACE activity is essential for local Ang II accumulation, stimulation of sodium transport in the distal nephron, and the induction of hypertension in response to hypertensive stimuli.

Cite This Study

González-Villalobos et al. (2013) studied this question.

synapsesocial.com/papers/6a717684ac440176ef2a27echttps://doi.org/10.1172/jci65460

Topics

Hypertension management
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