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(Circulation. 1999;100:1923-1929.)
© 1999 American Heart Association, Inc.

Basic Science Reports

Chromosomal Mapping of Quantitative Trait Loci That Influence Renal Hemodynamic Functions

Naoharu Iwai, MD, PhD; Masahiko Kinoshita, MD, PhD; Hitoshi Shimoike, MD, PhD

From the Research Institute, National Cardiovascular Center (N.I.) Osaka, and the First Department of Internal Medicine, Shiga University of Medical Sciences (M.K., H.S.), Ohtsu-city, Shiga-ken, Japan.

Correspondence to Naoharu Iwai, MD, Research Institute, National Cardiovascular Center, 5-7-1 Fujishirodai, Suita 565-8565, Osaka, Japan. E-mail niwai{at}res.ncvc.go.jp

Background—Impaired renal hemodynamic function has been suspected to be responsible for hypertension in the spontaneously hypertensive rat (SHR).

Methods and Results—We measured renal hemodynamic functions, including the glomerular filtration rate, renal plasma flow, and renal vascular resistance, in an F2 rat population derived from spontaneously hypertensive and Wistar-Kyoto (WKY) rats and performed a genome-wide screening to map quantitative trait loci that influence these functions to gain insight into the relationship between renal hemodynamic functions and blood pressure control. The D1 Mit7 locus was identified as a major locus that influenced renal hemodynamic functions, and we transferred the SHR chromosomal segment around the D1 Mit7 locus into the WKY strain. The congenic rats exhibited impaired renal hemodynamic functions. The systolic blood pressure of the congenic rats was significantly higher than that of age-matched WKY rats, but only at nighttime. No significant differences in systolic blood pressure during daytime or diastolic blood pressure were observed between the 2 strains

Conclusions—We have identified a chromosome segment that influences renal hemodynamic function. The SHR chromosome segment around the D1 Mit7 locus had significant, but not dramatic, effects in increasing blood pressure in the WKY genetic background. However, further studies will be necessary to determine the significance of this locus in SHR hypertension.

Key Words: hypertension • genetics • kidney

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