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It was initially postulated to be a compensatory mechanism to the blood pressure lowering effect of GLP-1 RAs that was possibly mediated by their vasodilatory effect [9, 31] and/or increased urinary sodium excretion [32]

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With this in mind, we explored the GEP44-mediated internalization of Y2-R and internalization and recruitment of -arrestin-2 at GLP-1R (Fig

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