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 hypertrophyper sedo 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.
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