Title : Ablation of the Cl-/HCO3- Exchanger Pendrin Enhances Hydrochlorothiazide-Induced Diuresis.

Pub. Date : 2017

PMID : 28750403






8 Functional Relationships(s)
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1 Ablation of the Cl-/HCO3- Exchanger Pendrin Enhances Hydrochlorothiazide-Induced Diuresis. Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus
2 We hypothesized that deletion of pendrin leaves NCC as the major salt absorbing transporter in the distal nephron and therefore enhances salt excretion by hydrochlorothiazide (HCTZ). Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus
3 We hypothesized that deletion of pendrin leaves NCC as the major salt absorbing transporter in the distal nephron and therefore enhances salt excretion by hydrochlorothiazide (HCTZ). Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus
4 Urine output and water intake increased significantly only in pendrin KO mice in response to HCTZ, but not in WT or NCC KO mice. Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus
5 Sodium and chloride excretion increased in HCTZ-treated pendrin KO mice, but they remained unchanged in WT or NCC KO mice. Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus
6 Pendrin KO mice treated with HCTZ developed volume depletion, as determined by increased expression of renin mRNA and protein. Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus
7 The expression of ENaC and pendrin increased in HCTZ-treated WT mice. Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus
8 CONCLUSION: The ablation of the Cl-/HCO3- exchanger Pendrin enhances the magnitude of salt wasting by HCTZ. Hydrochlorothiazide solute carrier family 26, member 4 Mus musculus