Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Carbohydrate doai
Patent
1984-11-26
1988-11-29
Griffin, Ronald W.
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Carbohydrate doai
514474, 514819, 514869, 424153, 424154, 424156, 424476, A61K 922, A61K 3308, A61K 3306
Patent
active
047881801
DESCRIPTION:
BRIEF SUMMARY
BACKGROUND OF THE INVENTION
This invention relates to pharmaceutical compositions comprising magnesium compounds.
In man and in animals (see Williams RJP, Wacker WEC, Cation Balance in Biological Systems, J. Amer. Med. Ass. 1967; 201/1: 96-100) intracellular concentrations of the four principal cations, sodium, potassium, magnesium and calcium, are in equilibrium such that log concentration ratios of the divalent cations magnesium and calcium are directly related to those for the monovalent cations potassium and sodium: total intracellular concentrations of sodium plus potassium and of magnesium plus calcium are respectively similar to those in extracellular fluid, and thus are similar on both sides of the cell membrane.
In man and in animals (Bloch M., Magnesium Depletion: Possible Significance in Ischaemic Heart Disease, Brit. J. Hosp. Med. 1973; 91-98) magnesium depletion results in negative magnesium and potassium balance, and positive sodium, calcium, and water balance; in intracellular loss of magnesium and potassium, and gain in sodium and calcium; in increase in extracellular fluid space; and in hypomagnesaemia, hypokalaemia, and hypocalcaemia. All these changes are reversible with
I have postulated that normal vascular muscle tone, a major determinant of normal blood pressure, is critically dependent on cation balance; that magnesium plays a signficiant role in blood pressure control; and that cation imbalance resulting from magnesium depletion, leading to relative and absolute increase in intracellular and total body calcium and sodium, and to decrease in intracellular and total body magnesium and potassium, would be expected to result in increase in vascular muscle tone and in blood pressure. In support of this hypothesis, it was noted also that magnesium depletion has been observed in association with increase in renal, cardiac, and skeletal-muscle calcification in animals, and that increase in myocardial calcium content has been reported in magnesium-deficient hearts of patients with ischaemic heart disease.
Further support for this hypothesis comes from recent observations in normal subjects and in patients with essential hypertension, linking increase in blood pressure to change in cation balance, these indicating variously 1227-29. Sodium and potassium in essential hypertension. Brit. Med. J. 1981; 283: 463-468) sodium content, and negatively with total-body potassium, plasma potassium concentration, and cellular efflux-rate of sodium; and that increase in blood pressure can be produced by increase in dietary sodium, and decrease in blood pressure by increase in dietary potassium Re-analysis of data in two Lancet papers on the effect of dietary sodium and potassium on blood pressure. Lancet 1981; ii: 1384-87. blood pressure in normal subjects. Lancet 1982; ii: 1127-29. potassium supplementation in essential hypertension. Lancet 1982; ii: 567-570.). hypomagnesaemia, and hypokalaemia, alone and in combination, mean systolic and diastolic blood pressure increased; local hypermagnesaemia is associated with decrease in resistance in forelimb, kidney, coronary, gastric, mesenteric and hepatic vascular beds in the dog and in the human forearm (see Emerson, TE, Scott JB, Haddy FJ., Effects of acute multiple changes in plasma electrolyte levels on dog blood pressure., Am. J. Physiol. 1970; 218/1: 234-240). In cats treated intravenously with magnesium, resultant fall in heart rate and in diastolic and systolic blood pressure were dose-dependent and correlated negatively with plasma magnesium concentration (see Ebel H, Classen HG, Marquardt P, Spaeth M., Zur Pharmakologie und Pharmakokinetik von Magnesium, Muench. Med. Wochenschr. 1975; 117/29-30: 1243-48). It is argued in the Editorial in Lancet 1982; ii: 965-967, cited above, that increase in vascular muscle tone might result from increase in free intracellular calcium; that abnormality of sodium transport does not have a primary role in genesis of essential hypertension; and that cation changes observed in essential hypertension reflect an unident
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patent: 3843778 (1974-10-01), Diamond et al.
patent: 4104370 (1978-08-01), Bloch
patent: 4150111 (1979-04-01), Warren et al.
patent: 4421743 (1983-12-01), Alvarez
patent: 4446135 (1984-05-01), Fountaine
patent: 4533543 (1985-08-01), Morris et al.
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