Key result
Intracerebroventricular infusion of human prorenin in a transgenic mouse model overexpressing human PRR in neurons increased blood pressure via an ANG II-independent, PRR-ERK-NOX4 mechanism.
Why the study?
Does intracerebroventricular infusion of human prorenin increase blood pressure via an angiotensin II-independent mechanism in mice overexpressing neuronal human (pro)renin receptor?
Population
Transgenic mouse model overexpressing human (pro)renin receptor (hPRR) specifically in neurons (Syn-hPRR)
Design
Preclinical
Authors
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Highlights potential new hypertension target in mice; hypothesis-generating and should not yet change practice.
Does intracerebroventricular infusion of human prorenin increase blood pressure via an angiotensin II-independent mechanism in mice overexpressing neuronal human (pro)renin receptor?
The study identifies a novel angiotensin II-independent mechanism for central blood pressure regulation mediated by human prorenin and the (pro)renin receptor via a PRR-ERK-NOX4 pathway.
Peng et al. (2017) studied Blood pressure regulation. Intracerebroventricular infusion of human prorenin was evaluated on Blood pressure response. Intracerebroventricular infusion of human prorenin in a transgenic mouse model overexpressing human PRR in neurons increased blood pressure via an ANG II-independent, PRR-ERK-NOX4 mechanism.