Effect of Feeding Various Levels of Calcium, Potassium and Magnesium to Rats

Colby, R. W.; Frye, Cheridah M.

doi:10.1152/ajplegacy.1951.166.1.209

Cited by 32 publications

(3 citation statements)

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“…Increased urinary Mg excretion and hypomagnesemia in our Ca-supplemented rats are compatible with earlier studies showing that a high-Ca diet lowers serum Mg concentration [35] and increases the severity of Mg deficiency [36]. Studies by Altura and Altura [37] indi cate that reduced extracellular Mg concentration causes constriction of isolated blood vessels, perhaps by allow ing the binding of more Ca to the vascular smooth muscle cell membrane.…”

Section: Calcium and Reduced Renal Masssupporting

confidence: 90%

Effect of increased dietary calcium on the development of reduced renal mass saline hypertension in rats.

Pamnani

Chen²,

Bryant³

et al. 1990

Journal of the American College of Nutrition

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A diet fortified with calcium carbonate has been reported to reduce blood pressure in low-renin and salt-sensitive hypertensive patients. We have therefore examined the effect of increased dietary calcium on the development of reduced renal mass-saline hypertension in rats, a classical, low-renin, volume, and sodium-dependent model of hypertension. Rats with 70-75% reduction in renal mass were divided into experimental and control groups. The experimental rats were fed a sodium-free diet supplemented with calcium carbonate (2.0% calcium) and drank 1% saline for 5 weeks. Control rats consumed the salt-free diet and drank 1% saline for the same period. In control rats, as previously observed, blood pressure progressive increased from a control value of 120.0 +/- 1.2 to 174.2 +/- 1.2 mm Hg by the fifth week. In contrast, in the calcium-supplemented rats the development of hypertension was significantly attenuated; the blood pressure only increased from 117.0 +/- 1.2 to 134.0 +/- 3.8 mm Hg by the fifth week. This was associated with a 30% decrease in saline intake by the fifth week, with proportionate decreases in urine volume and sodium excretion but not potassium excretion. Urinary magnesium excretion increased. No such changes were seen in control rats. At the end of the treatment period, plasma levels of sodium, potassium, calcium, creatinine, BUN, and protein were not different, but plasma chloride and magnesium were lower in experimental rats; vascular smooth muscle cell membrane potentials were also not different. These data show that dietary calcium carbonate can attenuate the development of reduced renal mass-saline hypertension in the rat, possibly in part by altering sodium and water intake.

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Section: Calcium and Reduced Renal Masssupporting

confidence: 90%

Effect of increased dietary calcium on the development of reduced renal mass saline hypertension in rats.

Pamnani

Chen²,

Bryant³

et al. 1990

Journal of the American College of Nutrition

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“…Correction of Κ deficiency appeared to uncover neuromuscular symptoms and signs just as in the index patient. A high Κ intake enhances Mg deficiency in rats [5].…”

Section: Hypomagnesemia and Hypokalemiamentioning

confidence: 99%

“…His sensorium cleared in 36 hours and remained clear thereafter. The fact that he had convulsions after calcium therapy has its counteφart in experimental Mg deficiency [5,6].…”

Section: Hypomagnesemia and Hypokalemiamentioning

confidence: 99%

Magnesium deficiency in human subjects—a personal historical perspective.

Flink¹

1985

Journal of the American College of Nutrition

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Over the past 30 years human magnesium (Mg) deficiency has become an accepted fact in most medical circles. Our index patient had striking neurological manifestations including generalized tremulousness, grimaces and fibrillary twitches of facial muscles, athetoid and choreiform movements of upper extremities, dysphagia, inability to speak, repeated convulsions, and confusion. She had received glucose in water and saline intravenously for several months. A patient with chronic alcoholism was noted to have almost identical symptoms and signs as the index patient. He also responded dramatically to MgSO4 injections. This resulted in a series of studies on patients with chronic alcoholism. The evidence of Mg deficiency in alcoholism includes the following: significant hypomagnesemia, strongly positive Mg balance during recovery, significant decrease in muscle Mg, a deficit of total exchangeable 28Mg quantitatively similar to deficit by balance studies, often a dramatic response of symptoms to therapy with Mg, and diuresis of Mg produced by ingestion of alcohol. Lipolysis with high levels of long-chain free fatty acids (FFA) occurs in withdrawal of alcohol in chronic alcoholism, withdrawal of certain addictive drugs, after trauma, surgery, administration of adrenergic compounds or theophylline, exposure to cold, and an adverse environment as in grass staggers. Concentrations of Mg fall when FFA increase in all of the above circumstances. This phenomenon has wide implications in health and disease. Better awareness of Mg deficiency in a wide variety of clinical conditions will result in life-saving treatment and less morbidity of other patients.

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