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Physiol. Genomics (November 15, 2001). doi:10.1152/physiolgenomics.00057.2001
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Articles in PresS, published online ahead of print November 15, 2001
Physiol Genomics, 10.1152/physiolgenomics.00057.2001
Submitted on July 13, 2001
Accepted on November 12, 2001

Chromosome 1 blood pressure QTL region influences renal function curve and salt sensitivity in SHR

Ming Lo1*, Kiao L Liu1, Jennifer-Rebecca Clemitson2, Jean Sassard1, and Nilesh J Samani2

1 Department of Physiology and Clinical Pharmacology, CNRS UMR 5014, Faculty of Pharmacy, Lyon, France
2 Department of Cardiology, Glenfield General Hospital, University of Leicester, Leicester, United Kingdom

* To whom correspondence should be addressed. E-mail: mlo{at}rockefeller.univ-lyon1.fr.

One or more quantitative trait locus (QTL) for blood pressure exists on rat chromosome 1, in the vicinity of the Sa gene. The present work examined whether this QTL region: 1) alters pressure-natriuresis relationship and 2) affects the BP response to salt load. Male spontaneously hypertensive rats (SHR), Wistar-Kyoto (WKY) rats and rats from an SHR congenic strain which contains a WKY chromosome 1 segment spanning the BP QTL region (SHR.WKY-Sa), were used. In an acute study in anaesthetized animals, renal function was measured at several levels of renal perfusion pressure. In a chronic study, BP was measured in freely moving rats using telemetry during normal and high sodium intake (2% NaCl as drinking water for 2 weeks). WKY rats showed a significantly higher glomerular filtration rate and increased pressure-natriuresis compared with SHR. SHR.WKY-Sa also demonstrated an increased glomerular filtration rate and enhanced pressure-natriuresis, associated with a lower tubular sodium reabsorption, compared with SHR. These modifications were accompanied by a lower basal BP in SHR.WKY-Sa compared with SHR and a markedly reduced BP response to salt load. These findings suggest that the BP QTL(s) present in this region of chromosome 1, influence BP and salt sensitivity, at least partly, by modulating pressure-natriuresis.




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