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大鼠心脏和肾脏肥大中的血管紧张素受体

Angiotensin receptors in cardiac and renal hypertrophy in rats.

作者信息

Brown L, Passmore M, Duce B, Sernia C

机构信息

Department of Physiology and Pharmacology, The University of Queensland 4072, Australia.

出版信息

J Mol Cell Cardiol. 1997 Nov;29(11):2925-9. doi: 10.1006/jmcc.1997.0527.

Abstract

Angiotensin II mediates its effects through activation of specific angiotensin (AT) receptors which can be regulated during cardiovascular disease. This study has investigated whether an increased cardiac and renal AT receptor density is important in the development of left ventricular and renal hypertrophy in three rat models of hypertension [spontaneous hypertensive (SHR), deoxycorticosterone acetate (DOCA)-salt and 2K1C renal hypertensive rats]. Although all hypertensive rats developed left ventricular and renal hypertrophy, AT receptor density increased only in the left ventricle and kidney of SHR during the development of hypertension. Thus, cardiac and renal hypertrophy per se do not increase AT receptor density. AT receptors were increased in the liver of DOCA-salt rats, 2K1C rats and 52-week-old SHR and in adrenal glands of DOCA-salt rats and SHR. A plausible explanation for tissue-dependent AT receptor regulation involves tissue-selective control of local renin-angiotensin systems independent of circulating hormone levels, combined with disease-induced cell damage.

摘要

血管紧张素II通过激活特定的血管紧张素(AT)受体介导其作用,这些受体在心血管疾病期间可受到调节。本研究调查了在三种高血压大鼠模型[自发性高血压(SHR)、醋酸脱氧皮质酮(DOCA)-盐和二肾一夹(2K1C)肾性高血压大鼠]中,心脏和肾脏AT受体密度增加在左心室和肾脏肥大发展过程中是否重要。尽管所有高血压大鼠均出现左心室和肾脏肥大,但在高血压发展过程中,仅SHR的左心室和肾脏中AT受体密度增加。因此,心脏和肾脏肥大本身并不会增加AT受体密度。DOCA-盐大鼠、2K1C大鼠和52周龄SHR的肝脏以及DOCA-盐大鼠和SHR的肾上腺中AT受体增加。对于组织依赖性AT受体调节的一个合理的解释是,涉及独立于循环激素水平的局部肾素-血管紧张素系统的组织选择性控制,以及疾病诱导的细胞损伤。

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