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Sympathetically mediated α1‐adrenoceptor regulation of the NCC during high salt intake to drive renal sodium retention: A new therapeutic anti‐hypertensive target?

It has been hypothesized that there is a direct role of increased sympathetic nervous system (SNS) release of norepinephrine (NE) in the up regulation of the sodium chloride cotransporter (NCC), via a β‐adrenoceptor pathway, to evoke the pathophysiology of salt sensitive hypertension (HTN). Recent data challenge this hypothesis and acute studies have suggested a potential role of α1 adrenoceptors in NCC regulation.