Transgenic mouse models of angiotensin receptor subtype function in the cardiovascular system

被引:19
作者
Brede, M [1 ]
Hein, L [1 ]
机构
[1] Univ Wurzburg, Inst Pharmakol & Toxikol, D-97078 Wurzburg, Germany
关键词
transgenic mouse model; angiotensin receptor; cardiovascular system;
D O I
10.1016/S0167-0115(00)00168-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Angiotensin II mediates is biological actions via different subtypes of G protein-coupled receptors, termed AT(1) and AT(2) receptors. In rodents, two AT(1) receptors have been identified, AT(1A) and AT(1B), whereas in humans a single AT(1) receptor exists. Recently, a number of transgenic animal models have been generated which overexpress or lack functional angiotensin II receptor subtypes. This review focuses on the physiological significance of angiotensin II receptor subtype diversity in the cardiovascular system. In the mouse, AT(1A) receptors are the major regulators of cardiovascular homeostasis by determining vascular tone and natriuresis. In addition, AT(1A) receptors mediate growth-stimulating signals in vascular and cardiac myocytes. AT(1B) receptors participate in blood pressure regulation, and their functions become apparent when the AT(1A) receptor gene is deleted. Deletion of the mouse gene for the AT(2) receptor subtype led to hypersensitivity to presser and antinatriuretic effects of angiotensin II in vivo, suggesting that the AT(2) receptor subtype counteracts some of the biological effects of AT(1) receptor signalling. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:125 / 132
页数:8
相关论文
共 59 条
  • [1] Increased vasoconstrictor response of the mouse lacking angiotensin II type 2 receptor
    Akishita, M
    Yamada, H
    Dzau, VJ
    Horiuchi, M
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 261 (02) : 345 - 349
  • [2] Expression of the AT2 receptor developmentally programs extracellular signal-regulated kinase activity and influences fetal vascular growth
    Akishita, M
    Ito, M
    Lehtonen, YA
    Daviet, L
    Dzau, VJ
    Horiuchi, M
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (01) : 63 - 71
  • [3] DIFFERENTIAL EXPRESSION OF ANGIOTENSIN RECEPTOR 1A AND 1B IN MOUSE
    BURSON, JM
    AGUILERA, G
    GROSS, KW
    SIGMUND, CD
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 267 (02): : E260 - E267
  • [4] Targeting deletion of angiotensin type 1B receptor gene in the mouse
    Chen, XM
    Li, WG
    Yoshida, H
    Tsuchida, S
    Nishimura, H
    Takemoto, F
    Okubo, S
    Fogo, A
    Matsusaka, T
    Ichikawa, I
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 1997, 272 (03) : F299 - F304
  • [5] IDENTIFICATION OF ANGIOTENSIN-II RECEPTOR SUBTYPES
    CHIU, AT
    HERBLIN, WF
    MCCALL, DE
    ARDECKY, RJ
    CARINI, DJ
    DUNCIA, JV
    PEASE, LJ
    WONG, PC
    WEXLER, RR
    JOHNSON, AL
    TIMMERMANS, PBMWM
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 165 (01) : 196 - 203
  • [6] Gene targeting in physiological investigations: Studies of the renin-angiotensin system
    Coffman, TM
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 1998, 274 (06) : F999 - F1005
  • [7] The cardiac renin-angiotensin system - Conceptual, or a regulator of cardiac function?
    Dostal, DE
    Baker, KM
    [J]. CIRCULATION RESEARCH, 1999, 85 (07) : 643 - 650
  • [8] TISSUE-SPECIFIC EXPRESSION OF TYPE-1 ANGIOTENSIN-II RECEPTOR SUBTYPES - AN IN-SITU HYBRIDIZATION STUDY
    GASC, JM
    SHANMUGAM, S
    SIBONY, M
    CORVOL, P
    [J]. HYPERTENSION, 1994, 24 (05) : 531 - 537
  • [9] Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors
    Hamawaki, M
    Coffman, TM
    Lashus, A
    Koide, M
    Zile, MR
    Oliverio, MI
    DeFreyte, G
    Cooper, G
    Carabello, BA
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1998, 274 (03): : H868 - H873
  • [10] Angiotensin II type 1A receptor knockout mice display less left ventricular remodeling and improved survival after myocardial infarction
    Harada, K
    Sugaya, T
    Murakami, K
    Yazaki, Y
    Komuro, I
    [J]. CIRCULATION, 1999, 100 (20) : 2093 - 2099