Physiol. Genomics AJP: Heart and Circulatory Physiology
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Physiol. Genomics 7: 171-177, 2001. First published October 30, 2001; doi:10.1152/physiolgenomics.00059.2001
1094-8341/01 $5.00
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Received 20 July 2001; accepted in final form 30 October 2001.
Physiological Genomics 7:171-177 (2001)
1094-8341/01 $5.00 © 2001 American Physiological Society

Replacement of {alpha}1-Na-K-ATPase of Dahl rats by Milan rats lowers blood pressure but does not affect its activity

SERGEI N. ORLOV1,2, JULIE DUTIL1, PAVEL HAMET1 and ALAN Y. DENG1

1 Research Centre, Centre Hospitalier de l’Université de Montreal, Hôtel Dieu, Montreal, Quebec, H2W 1T8, Canada
2 Department of Biomembranes, Faculty of Biology, Moscow State University, 119899 Moscow, Russia

Both linkage and use of congenic strains have shown that a chromosome region near the gene for the Na-K-ATPase {alpha}1-subunit (Atp1a1) contained a quantitative trait locus (QTL) for blood pressure (BP). 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 {alpha}1-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 {alpha}1-Na-K-ATPase activity or its stoichiometry. Atp1a1 is not supported as a candidate to be a BP QTL.

quantitative trait loci; genetic hypertension; telemetry




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