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Zn 2+  deficiency (ZnD) is a common comorbidity of many chronic diseases. In these settings, ZnD exacerbates hypertension. Whether ZnD alone is sufficient to alter blood pressure (BP) is unknown. To explore the role of Zn 2+  in BP regulation, adult mice were fed a Zn 2+ -adequate (ZnA) or a Zn 2+ -deficient (ZnD) diet. A subset of ZnD mice were either returned to the ZnA diet or treated with hydrochlorothiazide (HCTZ), a Na + -Cl −  cotransporter (NCC) inhibitor. To reduce intracellular Zn 2+  in vitro, mouse distal convoluted tubule cells were cultured in N,N,N′,N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN, a Zn 2+  chelator)- or vehicle (DMSO)-containing medium. To replete intracellular Zn 2+ , TPEN-exposed cells were then cultured in Zn 2+ -supplemented medium. ZnD promoted a biphasic BP response, characterized by episodes of high BP. BP increases were accompanied by reduced renal Na +  excretion and NCC upregulation. These effects were reversed in Zn 2+ -replete mice. Likewise, HCTZ stimulated natriuresis and reversed BP increases. In vitro, Zn 2+  depletion increased NCC expression. Furthermore, TPEN promoted NCC surface localization and Na +  uptake activity. Zn 2+  repletion reversed TPEN effects on NCC. These data indicate that 1) Zn 2+  contributes to BP regulation via modulation of renal Na +  transport, 2) renal NCC mediates ZnD-induced hypertension, and 3) NCC is a Zn 2+ -regulated transporter that is upregulated with ZnD. This study links dysregulated renal Na +  handling to ZnD-induced hypertension. Furthermore, NCC is identified as a novel mechanism by which Zn 2+  regulates BP. Understanding the mechanisms of ZnD-induced BP dysregulation may have an important therapeutic impact on hypertension.

Zinc deficiency induces hypertension by promoting renal Na+ reabsorption

Zinc deficiency induces hypertension by promoting renal Na⁺ reabsorption