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Effects of high sodium intake on cardiovascular aldosterone synthesis in stroke-prone spontaneously hypertensive rats

Takeda, Yoshiyua,b; Yoneda, Takashia; Demura, Masashia; Furukawa, Kenjia; Miyamori, Isamuc; Mabuchi, Hiroshia

Original papers: Heart

Objectives: Aldosterone is synthesized in extra-adrenal tissues such as the vasculature, heart and brain. The mechanisms underlying the effect of high salt intake on the development and acceleration of vascular injury and cardiac hypertrophy in the stroke-prone spontaneously hypertensive rats (SHRSP) are still not clear. The goal of this study was to determine whether high salt intake increases cardiovascular aldosterone synthesis in SHRSP.

Methods: Four-week-old SHRSP were given tap water or 0.9% NaCl solution for hydration for 4 weeks in addition to a normal salt diet. Isolated rat mesenteric arteries and hearts were perfused for 2 h, and the perfusate was analysed by high-performance liquid chromatography. The concentrations of aldosterone synthase gene (CYP11B2) mRNA and angiotensin II receptor (AT1R) mRNA were determined by competitive polymerase chain reaction.

Results: Salt-loaded SHRSP had higher blood pressures than SHRSP with normal salt intake. Plasma aldosterone concentrations and plasma renin activity were decreased by high salt intake. Aldosterone production, the expression of CYP11B2 mRNA and AT1R mRNA in mesenteric arteries and hearts were significantly increased by high salt intake.

Conclusions: These results suggest that high salt intake increases aldosterone production and expression of the AT1R mRNA in the cardiovascular tissue in SHRSP, which may contribute to the development of malignant hypertension in salt-loaded SHRSP.

aSecond Department of Internal Medicine, bDepartment of Health Sciences, School of Medicine, Kanazawa University, Kanazawa, Japan and cThird Department of Internal Medicine, Fukui Medical School, Fukui, Japan.

Sponsorship: This work was supported in part by Grants-in-Aid for Scientific Research from the Ministry of Education, Science and Culture, Japan and Yamanouchi Foundation for Research on Metabolic Disorders.

Correspondence and requests for reprints to Yoshiyu Takeda, Second Department of Internal Medicine, School of Medicine, Kanazawa University, 13–1 Takara-machi, Kanazawa 920, Japan. Tel: + 81 76 265 2252; fax: +81 76 234 4251; e-mail:

© 2001 Lippincott Williams & Wilkins, Inc.