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Physiol. Genomics (October 30, 2001). doi:10.1152/physiolgenomics.00059.2001
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Articles in PresS, published online ahead of print October 29, 2001
Physiol Genomics, 10.1152/physiolgenomics.00059.2001
Submitted on July 20, 2001
Accepted on October 25, 2001

Replacement of a1 Na/K-ATPase of Dahl rats by Milan rats lowers blood pressure but does not affect its activity

Sergei N Orlov1, Julie Dutil2, Pavel Hamet2, and Alan Y Deng2*

1 Medicine, Research Centre-CHUM, Montreal, Quebec, Canada; Biomembranes, Moscow State University, Moscow, Russian Federation
2 Medicine, Research Centre-CHUM, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: alan.deng{at}umontreal.ca.

Both linkage and use of congenic strains have shown that a chromosome region near the gene for the {alpha}1 Na/K-ATPase subunit (Atp1a1) contained a quantitative trait locus (QTL) for blood pressure. Currently, two congenic strains, designated S.M5 and S.M6, were made by replacing a segment of the Dahl salt-sensitive SS/Jr (S) rat by the homologous region of the Milan normotensive rat (MNS). In S.M5, the gene for Atp1a1 is from the MNS strain; whereas in S.M6, Atp1a1 is from the S strain. The baseline activity of the a1 Na/K-ATPase and its stoichiometry were evaluated by an assay of ouabain-sensitive inwardly and outwardly directed 86Rb and 22Na fluxes in erythrocytes. The two congenic strains showed a similar BP, but both had a BP lower than that of S rats (p<0.0001). Neither the {alpha}1 Na/K-ATPase activity nor its stoichiometry was affected by the substitution of the Atp1a1 alleles of S by those of MNS. Thus, the BP-lowering effects observed in S.M5 and S.M6 could not be attributed to the a Na/K-ATPase activity or its stoichiometry. Atp1a1 is not supported as a candidate to be a BP QTL.




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