QTL associated with blood pressure, heart rate, and heart weight in CBA/CaJ and BALB/cJ mice

被引:46
作者
Sugiyama, F
Churchill, GA
Li, RH
Libby, LJM
Carver, T
Yagami, KI
John, SWM
Paigen, B
机构
[1] Jackson Lab, Bar Harbor, ME 04609 USA
[2] Howard Hughes Med Inst, Bar Harbor, ME 04609 USA
[3] Univ Tsukuba, Lab Anim Resource Res Ctr, Tsukuba, Ibaraki 3058575, Japan
关键词
quantitative trait loci; hypertension;
D O I
10.1152/physiolgenomics.00002.2002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
To better understand the genetic basis of essential hypertension, we conducted a quantitative trait locus (QTL) analysis of a population of 207 (BALB/cJ x CBA/CaJ) F-2 male mice to identify genomic regions that regulate blood pressure, heart rate, and heart weight. We identified two loci, Bpq6 (blood pressure quantitative locus 6) on chromosome 15 (Chr 15; peak, 16 cM; 95% confidence interval, 0-25 cM) and Bpq7 on Chr 7 (peak, 42 cM; 95% confidence interval, 35-50 cM) that were significantly associated with blood pressure. We also identified two loci, Hrq1 (heart rate quantitative locus 1) and Hrq2, on D2Mit304 (peak, 72 cM; 95% confidence interval 60-80 cM) and D15Mit184 (peak, 25 cM; 95% confidence interval 20-35 cM), respectively, that were significantly associated with heart rate. A significant gene-gene interaction for heart rate was found between Hrq1 and D1Mit10 (peak, 57 cM; 95% confidence interval, 45-75 cM); the latter QTL was named Hrq3. We identified a significant locus for heart weight, Hwq1 (heart weight quantitative locus 1), at D14Mit67 (peak, 38 cM; 95% confidence interval, 20-43 cM). Identification of the genes for these QTL should lead to a better understanding of the causes of essential hypertension.
引用
收藏
页码:5 / 12
页数:8
相关论文
共 34 条
[1]   Prevalence of insulin resistance in metabolic disorders - The Bruneck Study [J].
Bonora, E ;
Kiechl, S ;
Willeit, J ;
Oberhollenzer, F ;
Egger, G ;
Targher, G ;
Alberiche, M ;
Bonadonna, RC ;
Muggeo, M .
DIABETES, 1998, 47 (10) :1643-1649
[2]   PEPTIDES FROM THE CALCITONIN GENES - MOLECULAR-GENETICS, STRUCTURE AND FUNCTION [J].
BREIMER, LH ;
MACINTYRE, I ;
ZAIDI, M .
BIOCHEMICAL JOURNAL, 1988, 255 (02) :377-390
[3]  
Brown JH, 1996, GOODMAN GILMANS PHAR, P141
[4]  
CHURCHILL GA, 1994, GENETICS, V138, P963
[5]   LINKAGE OF 11-BETA-HYDROXYLASE MUTATIONS WITH ALTERED STEROID-BIOSYNTHESIS AND BLOOD-PRESSURE IN THE DAHL RAT [J].
CICILA, GT ;
RAPP, JP ;
WANG, JM ;
STLEZIN, E ;
NG, SC ;
KURTZ, TW .
NATURE GENETICS, 1993, 3 (04) :346-353
[6]   High-resolution mapping of the blood pressure QTL on chromosome 7 using Dahl rat congenic strains [J].
Cicila, GT ;
Garrett, MR ;
Lee, SJ ;
Liu, J ;
Dene, H ;
Rapp, JP .
GENOMICS, 2001, 72 (01) :51-60
[7]   MUTATIONS IN THE CYP11B1 GENE CAUSING CONGENITAL ADRENAL-HYPERPLASIA AND HYPERTENSION CLUSTER IN EXON-6, EXON-7, AND EXON-8 [J].
CURNOW, KM ;
SLUTSKER, L ;
VITEK, J ;
COLE, T ;
SPEISER, PW ;
NEW, MI ;
WHITE, PC ;
PASCOE, L .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (10) :4552-4556
[8]   Increased blood pressure in α-calcitonin gene-related peptide/calcitonin gene knockout mice [J].
Gangula, PRR ;
Zhao, HW ;
Supowit, SC ;
Wimalawansa, SJ ;
Dipette, DJ ;
Westlund, KN ;
Gagel, RF ;
Yallampalli, C .
HYPERTENSION, 2000, 35 (01) :470-475
[9]   HYPERTENSION CAUSED BY A TRUNCATED EPITHELIAL SODIUM-CHANNEL GAMMA-SUBUNIT - GENETIC-HETEROGENEITY OF LIDDLE SYNDROME [J].
HANSSON, JH ;
NELSONWILLIAMS, C ;
SUZUKI, H ;
SCHILD, L ;
SHIMKETS, R ;
LU, Y ;
CANESSA, C ;
IWASAKI, T ;
ROSSIER, B ;
LIFTON, RP .
NATURE GENETICS, 1995, 11 (01) :76-82
[10]   COEXPRESSION OF 4 MUSCARINIC RECEPTOR GENES BY THE INTRINSIC NEURONS OF THE RAT AND GUINEA-PIG HEART [J].
HASSALL, CJS ;
STANFORD, SC ;
BURNSTOCK, G ;
BUCKLEY, NJ .
NEUROSCIENCE, 1993, 56 (04) :1041-1048