Thiazide-Sensitive NCC (Sodium-Chloride Cotransporter) in Human Metabolic Syndrome

The thiazide-sensitive sodium-chloride cotransporter (NCC;SLC12A3) is central to sodium and blood pressure regulation. Metabolic syndrome induces NCC upregulation generating sodium-sensitive hypertension in experimental animal models. We tested the role of sensitivity hypertensive humans with metabolic syndrome. Conversely, oral potassium downregulation producing potassium-induced natriuresis. determined time course magnitude natriuresis compared following hydrochlorothiazide (HCTZ) as a reference standard. studied 19 obese during 13-day inpatient confinement. by change 24-hour mean systolic automated monitor from days 5 (low sodium) 10 (high sodium). activity standard 50 mg HCTZ test (day 11). 35 mmol KCl 13). (1) whether was greater versus sodium-resistant participants correlated (2) directly HCTZ. not did correlate sensitivity. Thirty-five-millimoles produced rapid approximately half that kaliuresis. Our investigation key hypothesis regarding human characterized In adults ingesting high-sodium diet, had net natriuretic effect