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Author Sapna, S. ♦ Ranjith, S. K. ♦ Shivakumar, K.
Source Sree Chitra Tirunal Institute for Medical Sciences & Technology
Content type Text
Publisher American Journal of Physiology-heart and Circulatory Physiology
File Format PDF
Language English
Subject Domain (in DDC) Natural sciences & mathematics ♦ Life sciences; biology ♦ Physiology & related subjects ♦ Biochemistry ♦ Technology ♦ Medicine & health
Subject Domain (in MeSH) Nutritional and Metabolic Diseases ♦ Diseases ♦ Hormones, Hormone Substitutes, and Hormone Antagonists ♦ Amino Acids, Peptides, and Proteins ♦ Biological Factors ♦ Chemicals and Drugs ♦ Chemical Phenomena ♦ Cell Physiological Phenomena ♦ Biological Sciences
Subject Keyword Biochemistry
Abstract Mechanisms underlying cardiac fibrogenesis in magnesium deficiency are unclear. It was reported earlier from this laboratory that serum from magnesium-deficient rats has a more pronounced stimulatory effect on cell proliferation, net collagen production, and superoxide generation in adult rat cardiac fibroblasts than serum from rats on the control diet. The profibrotic serum factors were, however, not identified. This study tested the hypothesis that circulating angiotensin II may modulate cardiac fibroblast activity in hypomagnesemic rats. Male Sprague-Dawley rats were pair-fed a magnesium-deficient ( 0.0008% Mg) or -sufficient ( 0.05%) diet for 6 days, and the effects of serum from these rats on [ H-3] thymidine and [ H-3] proline incorporation into cardiac fibroblasts from young adult rats were evaluated in the presence of losartan, an angiotensin II type 1 ( AT(1)) receptor antagonist, and spironolactone, an aldosterone antagonist. Losartan and spironolactone markedly attenuated the stimulatory effects in vitro of serum from the magnesium-deficient and control groups, but the inhibitory effects were considerably higher in cells exposed to serum from magnesium-deficient animals. Circulating and cardiac tissue levels of angiotensin II were significantly elevated in magnesium-deficient animals ( 67.6% and 93.1%, respectively, vs. control). Plasma renin activity was 61.9% higher in magnesium-deficient rats, but serum angiotensin-converting enzyme activity was comparable in the two groups. Furthermore, preliminary experiments in vivo using enalapril supported a role for angiotensin II in magnesium deficiency. There was no significant difference between the groups in serum aldosterone levels. The findings suggest that circulating angiotensin II and aldosterone may stimulate fibroblast activity and contribute to a fibrogenic response in the heart in magnesium deficiency.
Education Level UG and PG
Learning Resource Type Article
Educational Framework Medical Council of India (MCI)
Journal American Journal of Physiology-Heart and Circulatory Physiology
Volume Number 291
Issue Number 1