Neuronal AT1 receptors drive ADAM17-mediated ACE2 shedding in the brains of hypertensive patients, contributing to the pathophysiology of neurogenic hypertension.
Does not support clinical targeting of brain AT1 receptors; leaves open therapeutic relevance of the ADAM17-ACE2 axis in hypertension.
Our data demonstrate that angiotensin II type 1 receptors promote ADAM17-mediated ACE2 shedding in the brain of hypertensive patients, leading to a loss in compensatory activity during neurogenic hypertension.
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Xu et al. (2017) studied this question.
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