Key result
ACE2 gene transfer into the paraventricular nucleus attenuated renal sympathetic nerve activity responses to NOS inhibition in rats with chronic heart failure (16% vs 28%, P<0.05).
Why the study?
Does ACE2 gene transfer in the PVN improve central nitric oxide-mediated sympathetic outflow in rats with chronic heart failure?
Does ACE2 gene transfer in the PVN improve central nitric oxide-mediated sympathetic outflow in rats with chronic heart failure?
Absolute Event Rate: 16% vs 28%
p-value: p=<0.05
ACE2 overexpression in the paraventricular nucleus increases nNOS expression and reduces sympathetic outflow in a rat model of chronic heart failure.
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Supports targeting PVN ACE2 to modulate sympathetic outflow in experimental HF; leaves open translation to patients.
Zheng et al. (2011) studied Chronic heart failure (CHF). Adenovirus vectors encoding ACE2 (AdACE2) gene transfer vs. AdEGFP (control vector) was evaluated on Response of renal sympathetic nerve activity (RSNA) to NOS inhibitor N-monomethyl-L-arginine (p=<0.05). ACE2 gene transfer into the paraventricular nucleus attenuated renal sympathetic nerve activity responses to NOS inhibition in rats with chronic heart failure (16% vs 28%, P<0.05).
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