Key result
Overexpression of mito-ECFP/Ang II in mouse proximal tubule mitochondria increased systolic blood pressure by 12±3 mm Hg (P<0.01), an effect attenuated in PT-Agtr1a-/- and PT-Nhe3-/- mice.
Why the study?
To test whether mitochondrial overexpression of Ang II in mouse proximal tubule cells induces oxidative and glycolytic responses and elevates blood pressure via Ang II/AT1a receptor/superoxide/NHE3-dependent mechanisms.
p-value: p=<0.01
Overexpression of mitochondrial Ang II in kidney proximal tubules induces oxidative and glycolytic responses and elevates blood pressure, highlighting a physiological role for mitochondrial Ang II signaling in blood pressure homeostasis.
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Hypothesis-generating for mitochondrial Ang II in proximal tubule hypertension; human studies needed before clinical relevance.
Li et al. (2020) studied Blood pressure homeostasis. Overexpression of mito-ECFP/Ang II was evaluated on Systolic blood pressure (p=<0.01). Overexpression of mito-ECFP/Ang II in mouse proximal tubule mitochondria increased systolic blood pressure by 12±3 mm Hg (P<0.01), an effect attenuated in PT-Agtr1a-/- and PT-Nhe3-/- mice.
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