RGD Reference Report - Heterozygous disruption of renal outer medullary potassium channel in rats is associated with reduced blood pressure. - Rat Genome Database

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Heterozygous disruption of renal outer medullary potassium channel in rats is associated with reduced blood pressure.

Authors: Zhou, Xiaoyan  Zhang, Zuo  Shin, Myung Kyun  Horwitz, Sarah Beth  Levorse, John M  Zhu, Lei  Sharif-Rodriguez, Wanda  Streltsov, Denis Y  Dajee, Maya  Hernandez, Melba  Pan, Yi  Urosevic-Price, Olga  Wang, Li  Forrest, Gail  Szeto, Daphne  Zhu, Yonghua  Cui, Yan  Michael, Bindhu  Balogh, Leslie Ann  Welling, Paul A  Wade, James B  Roy, Sophie  Sullivan, Kathleen A 
Citation: Zhou X, etal., Hypertension. 2013 Aug;62(2):288-94. doi: 10.1161/HYPERTENSIONAHA.111.01051. Epub 2013 Jun 10.
RGD ID: 13782272
Pubmed: PMID:23753405   (View Abstract at PubMed)
DOI: DOI:10.1161/HYPERTENSIONAHA.111.01051   (Journal Full-text)

The renal outer medullary potassium channel (ROMK, KCNJ1) mediates potassium recycling and facilitates sodium reabsorption through the Na(+)/K(+)/2Cl(-) cotransporter in the loop of Henle and potassium secretion at the cortical collecting duct. Human genetic studies indicate that ROMK homozygous loss-of-function mutations cause type II Bartter syndrome, featuring polyuria, renal salt wasting, and hypotension; humans heterozygous for ROMK mutations identified in the Framingham Heart Study have reduced blood pressure. ROMK null mice recapitulate many of the features of type II Bartter syndrome. We have generated an ROMK knockout rat model in Dahl salt-sensitive background by using zinc finger nuclease technology and investigated the effects of knocking out ROMK on systemic and renal hemodynamics and kidney histology in the Dahl salt-sensitive rats. The ROMK(-/-) pups recapitulated features identified in the ROMK null mice. The ROMK(+/-) rats, when challenged with a 4% salt diet, exhibited a reduced blood pressure compared with their ROMK(+/+) littermates. More importantly, when challenged with an 8% salt diet, the Dahl salt-sensitive rats with 50% less ROMK expression showed increased protection from salt-induced blood pressure elevation and signs of protection from renal injury. Our findings in ROMK knockout Dahl salt-sensitive rats, together with the previous reports in humans and mice, underscore a critical role of ROMK in blood pressure regulation.



Phenotype Annotations    

Objects Annotated

Genes (Rattus norvegicus)
Kcnj1  (potassium inwardly-rectifying channel, subfamily J, member 1)
Kcnj1em1Kasu  (potassium voltage-gated channel subfamily J member 1; ZFN induced mutant 1,Kasu)

Objects referenced in this article
Strain SS-Kcnj1em1Kasu+/+ null Rattus norvegicus

Additional Information