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Calcium Modulation of Hypertension and Obesity: Mechanisms and Implications

Departments of Nutrition and Medicine, University of Tennessee, Knoxville, Tennessee

View larger version (17K): [in a new window]   Fig. 1. Mechanism of dietary calcium modulation of blood pressure. 1,25-(OH)2-D stimulates calcium influx into vascular smooth muscle cells, thereby increasing vascular tone and blood pressure. Dietary calcium reduces the stimulus for Ca2+ influx by suppressing 1,25-(OH)2-D production.

View larger version (17K): [in a new window]   Fig. 2. Role of renal calcium leak in essential hypertension. Hypertensives exhibit an increase in urinary calcium losses, which is exacerbated on high salt diets. This results in a transient decrease in serum ionized Ca2+. The parathyroid gland responds to this decrease with the release of parathyroid hormone (PTH), which activates the renal 1--hydroxylase, resulting in increased 1,25-(OH)2-D production. 1,25-(OH)2-D serves as a stimulus to increase vascular smooth muscle intracellular Ca2+.

View larger version (17K): [in a new window]   Fig. 3. Agouti modulation of adipocyte lipid metabolism. Agouti stimulates adipocyte Ca2+ influx. Increased adipocyte intracellular calcium ([Ca2+]i stimulates fatty acid synthase (FAS) transcription and activity, resulting in increased de novo lipogenesis, and also inhibits lipolysis. Consequently, adipocyte triglyceride stores are expanded.

View larger version (16K): [in a new window]   Fig. 4. Role of dietary calcium in modulating adipocyte lipid metabolism. 1,25-(OH)2-D stimulates adipocyte Ca2+ influx. This results in stimulation of fatty acid synthase (FAS) transcription and activity, increased de novo lipogenesis, and decreased lipolysis. Consequently, adipocyte triglyceride stores are expanded. Dietary calcium reduces the stimulus for Ca2+ influx by suppressing 1,25-(OH)2-D production, thereby permitting down-regulation of lipogenesis and up-regulation of lipolysis, resulting in reduced adipocyte triglyceride stores.