Why the study?
To investigate the role of calcineurin signaling in the paraventricular nucleus in sympathetic overactivity in spontaneously hypertensive rats.
RCAN1-mediated calcineurin hypoactivity in the paraventricular nucleus drives sympathetic overactivity in genetic hypertension, identifying a potential novel therapeutic target for neurogenic hypertension.
Hypothesis-generating for PVN calcineurin in sympathetic hypertension; leaves open translation beyond SHR models.
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Zhou et al. (2025) studied this question.
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