Key result
NOXA1 inhibition blunts acute angiotensin II-induced renal artery vasoconstriction in mice.
NOXA1/NOX1-mediated superoxide signaling plays a key role in angiotensin II-induced vasoconstriction, suggesting NOX1 inhibition as a potential therapeutic target for hypertension.
Hypothesis-generating for NOX1 inhibition in hypertension; clinical translation remains open pending human studies.
Renal reactivity to angiotensin II (ANG II) is mediated by superoxide signaling produced by NADPH oxidase (NOX)A1/NOX1. Acute vasoconstriction of renal arteries by ANG was blunted in Noxa1 −/− compared with wild-type mice. NOXA1/NOX1/O 2 •− signaling was also observed in ANG II stimulation of vascular smooth muscle cells and isolated mesenteric resistance arteries, indicating that it contributes to ANG II-induced hypertension. A NOXA1/NOX1 assembly inhibitor (C25) has been characterized that inhibits superoxide production and ameliorates the effects of ANG II.
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Stevenson et al. (2023) studied ANG II-induced hypertension. Noxa1 knockout / NOXA1/NOX1 assembly inhibitor (C25) vs. Wild-type mice was evaluated on Acute vasoconstriction of renal arteries and superoxide production. Acute vasoconstriction of renal arteries by angiotensin II was blunted in Noxa1 -/- mice compared with wild-type, and a NOXA1/NOX1 assembly inhibitor (C25) ameliorated the effects of ANG II.
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