Abstract
Salbutamol activates the NaCl cotransporter of the distal convoluted tubule. Salbutamol, in conjunction with high salt intake, induced hypertension in mice, rescued by thiazide therapy. Phosphoproteomics identified protein phosphatase 1/inhibitor 1 as a distinct regulatory node for NaCl cotransporter activation by salbutamol, which did not activate the transporter in inhibitor 1 knockout mice. Salbutamol is widely used in respiratory medicine, and the acquisition of salt sensitivity may be relevant to understanding cardiovascular risk in certain patients.
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