Key result
XNT enhanced blood pressure recovery in Ang II-induced hypertension (slope -3.26 vs -1.6 mm Hg/min; P<0.01), but this effect was ACE2-independent.
Why the study?
Do presumed ACE2 activators XNT and diminazene lower blood pressure via ACE2 activation in models of Ang II-induced hypertension?
Population
Wild-type mice, ACE2 knockout mice, and rat kidney models
Comparison
XNT (1-[ethylamino]-4--7-[ sulfonyl… vs Control (without XNT or diminazene)
Design
Preclinical
Authors
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Challenges presumed ACE2 activation by XNT/diminazene; leaves open alternative mechanisms in hypertension models.
Do presumed ACE2 activators XNT and diminazene lower blood pressure via ACE2 activation in models of Ang II-induced hypertension?
Absolute Event Rate: -3.26% vs -1.6%
p-value: p=<0.01
The blood pressure-lowering and biological effects of XNT and diminazene are independent of ACE2 activation, challenging previous assumptions that they act as ACE2 activators.
Haber et al. (2014) studied Ang II-induced acute hypertension. XNT vs. without XNT was evaluated on Blood pressure recovery slope (p=<0.01). XNT enhanced blood pressure recovery in Ang II-induced hypertension (slope -3.26 vs -1.6 mm Hg/min; P<0.01), but this effect was ACE2-independent.
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