Effect of Salvia miltiorrhiza on left ventricular hypertrophy and cardiac aldosterone in spontaneously hypertensive rats.
- Author:
Shaojie HAN
1
;
Zhi ZHENG
;
Dahong REN
Author Information
1. Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030.
- Publication Type:Journal Article
- MeSH:
Aldosterone;
metabolism;
Animals;
Drugs, Chinese Herbal;
pharmacology;
Hypertension;
metabolism;
physiopathology;
Hypertrophy, Left Ventricular;
metabolism;
prevention & control;
Male;
Myocardium;
metabolism;
Rats;
Rats, Inbred SHR;
Rats, Inbred WKY;
Salvia miltiorrhiza
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2002;22(4):302-304
- CountryChina
- Language:English
-
Abstract:
Chronic treatment with Salvia Miltiorrhiza preventing left ventricular hypertrophy (LVH) and its possible mechanism--inhibiting the action of cardiac aldosterone in spontaneously hypertensive rats (SHR) were investigated. Normotensive Wistar-kyoto (WKY) rats and SHRs were used. Part of SHRs was treated with Salvia Miltiorrhiza for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index were measured. Sections of heart tissue were stained with HE method and VanGieson method. Collagen volume fraction was determined in the left ventricle by automatically quantitative morphometry. Cardiac aldosterone concentration was measured by radioimmunoassay. The results indicated that compared with WKY rats, SHRs exhibited higher SBP, left ventricular collagen volume fraction, and aldosterone concentration (all P < 0.05). After the treatment with Salvia Miltiorrhiza, SBP, left ventricular collagen volume fraction, and aldosterone concentration in SHR were decreased as compared with control group (P < 0.05) except SBP. It was concluded that chronic treatment with Salvia Miltiorrhiza could prevent left ventricular hypertrophy in SHR, significantly inhibit collagen compositions in left ventricle. The mechanism was probably related with the inhibition of the cardiac aldosterone action.
