Published Online
on April 4, 2005

A more recent version of this article appeared on May 1, 2005

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Submitted on October 28, 2004
Revised on November 15, 2004

Klk1 as One of the Genes Contributing to Hypertension in Dahl Salt-Sensitive Rat

Naoharu Iwai^*; Naomi Yasui; Hiroaki Naraba; Naomi Tago; Hideyuki Yamawaki; and Hiroshi Sumiya

From the Research Institute, National Cardiovascular Center, Suita, Osaka, Japan.

^* To whom correspondence should be addressed. E-mail: iwai{at}ri.ncvc.go.jp.

Abstract--A genome-wide quantitative trait loci analysis for blood pressure was performed using 107 male F₂ rats derived from Dahl salt-sensitive and Lewis rats. Blood pressure was assessed by telemetry, and >400 microsatellite markers were used for genotyping. Two major quantitative trait loci for blood pressure were identified at chromosome 1 and chromosome 10. The expression levels of 366 transcripts around the chromosome 1 quantitative trait loci were assessed by RT-PCR, and we found that the Klk1 (kallikrein 1) and Ngfg (nerve growth factor gamma) mRNA levels were significantly reduced in the kidneys of Dahl salt-sensitive rats compared with those in Lewis rats. The expression levels of kallikrein 1 protein were also suppressed in Dahl salt-sensitive rats compared with those in Lewis rats. Because the kallikrein-kinin system has been shown to be involved in renal function, including salt homeostasis, it is likely that the reduced expression of Klk1 contributes to salt-sensitive hypertension in Dahl salt-sensitive rats.

Key words: kallikreins • rats, Dahl • genetics

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