Blood pressure, baroreflex sensitivity, and end organ damage in hybrid offspring of spontaneously hypertensive rats and Sprague-Dawley rats

被引:8
作者
Xie, HH [1 ]
Shen, FM [1 ]
Miao, CY [1 ]
Su, DF [1 ]
机构
[1] Second Mil Med Univ, Dept Pharmacol, Shanghai 200433, Peoples R China
关键词
baroreflex; blood pressure; end organ damage; hypertension; genetic hybridization;
D O I
10.1111/j.1745-7254.2005.00162.x
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
Aim: To investigate the blood pressure (BP), baroreflex sensitivity (BRS), and organ damage in hybrids of spontaneously hypertensive rats and Sprague-Dawley rats. Methods: Spontaneously hypertensive rats and Sprague-Dawley rats were crossbred, and the F-1 hybrids were inbred randomly to produce an F-2 generation. At the age of 52 weeks, the F-1 and F-2 hybrids were tested to determine BP and BRS in a conscious state. Histopathological examinations were carried out after BP recording and BRS studies. Results: BP and BRS were not different in F-1 and F-2 hybrids. BRS was inversely related to systolic BP (SBP) in male, female, or whole populations of hybrids. Quantitatively, BRS values were one-third determined by SBP level (the determinant coefficient was 0.326). The indexes for left ventricular hypertrophy, aortic hypertrophy, and renal damage were all positively related to BP, and negatively related to BRS. In multiple-regression analysis, left ventricular and aortic hypertrophy and glomerulosclerosis score were all most significantly associated with lower BRS and higher systolic BP. The contribution of BRS to left ventricular and aortic hypertrophy and glomerulosclerosis was greater than that of SBP. Conclusion: The present work with hybrid rats demonstrated quantitatively that the BRS value was one-third determined by SBP level. Both BP level and BRS value contributed greatly to the hypertensive organ damage. However, the contribution of BRS to the hypertensive organ damage was greater than that of BP level in these rats.
引用
收藏
页码:1049 / 1056
页数:8
相关论文
共 36 条
[1]  
BACHMANOV A A, 1989, Fiziologicheskii Zhurnal SSSR Imeni I M Sechenova, V75, P1714
[2]   DIMINISHED BAROREFLEX SENSITIVITY IN HIGH BLOOD PRESSURE [J].
BRISTOW, JD ;
HONOUR, AJ ;
PICKERING, GW ;
SLEIGHT, P ;
SMYTH, HS .
CIRCULATION, 1969, 39 (01) :48-+
[3]   BLOOD-PRESSURE IN GENETICALLY HYPERTENSIVE RATS - INFLUENCE OF THE Y-CHROMOSOME [J].
DAVIDSON, AO ;
SCHORK, N ;
JAQUES, BC ;
KELMAN, AW ;
SUTCLIFFE, RG ;
REID, JL ;
DOMINICZAK, AF .
HYPERTENSION, 1995, 26 (03) :452-459
[4]   Effects of long-term treatment with ketanserin on blood pressure variability and end-organ damage in spontaneously hypertensive rats [J].
Du, WM ;
Miao, CY ;
Liu, JG ;
Shen, FM ;
Yang, XQ ;
Su, DF .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2003, 41 (02) :233-239
[5]   CAROTID BAROREFLEX FUNCTION IN YOUNG MEN WITH BORDERLINE BLOOD-PRESSURE ELEVATION [J].
ECKBERG, DL .
CIRCULATION, 1979, 59 (04) :632-636
[6]   HYPERTENSION IN THE SPONTANEOUSLY HYPERTENSIVE RAT IS LINKED TO THE Y-CHROMOSOME [J].
ELY, DL ;
TURNER, ME .
HYPERTENSION, 1990, 16 (03) :277-281
[7]   THE HYPERTENSIVE Y-CHROMOSOME ELEVATES BLOOD-PRESSURE IN F11 NORMOTENSIVE RATS [J].
ELY, DL ;
DANESHVAR, H ;
TURNER, ME ;
JOHNSON, ML ;
SALISBURY, RL .
HYPERTENSION, 1993, 21 (06) :1071-1075
[8]   Cardiovascular hypertrophy does not predispose to genetic hypertension [J].
Harrap, SB ;
Jones, EF .
CLINICAL AND EXPERIMENTAL HYPERTENSION, 1997, 19 (5-6) :531-541
[9]   The link among nitric oxide synthase activity, endothelial function, and aortic and ventricular hypertrophy in hypertension [J].
Hayakawa, H ;
Raij, L .
HYPERTENSION, 1997, 29 (01) :235-241
[10]   DISSOCIATION OF GENETIC HYPERACTIVITY AND HYPERTENSION IN SHR [J].
HENDLEY, ED ;
ATWATER, DG ;
MYERS, MM ;
WHITEHORN, D .
HYPERTENSION, 1983, 5 (02) :211-217