Effect of oral magnesium supplementation on blood pressure, platelet aggregation and calcium handling in deoxycorticosterone acetate-induced hypertension in rats [2]

Journal of Hypertension

Volumn 19, Issue 1, 2001, Pages 161-162

  Kisters, Klaus ^a,b,c   Hausberg, Martin ^a,b   Kosch, Markus ^a,b  

^a RUHR UNIVERSITY BOCHUM   (Germany)

^b Medical University Policlinic   (Germany)

^c Medical Clinic i   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM; DEOXYCORTICOSTERONE ACETATE; MAGNESIUM;

ANIMAL EXPERIMENT; ANIMAL MODEL; BLOOD PRESSURE REGULATION; CALCIUM CELL LEVEL; DIET SUPPLEMENTATION; HYPERTENSION; ION EXCHANGE; LETTER; MAGNESIUM BLOOD LEVEL; MAGNESIUM DEFICIENCY; NONHUMAN; PRIORITY JOURNAL; RAT; THROMBOCYTE AGGREGATION;

EID: 0035139863     PISSN: 02636352     EISSN: None     Source Type: Journal    
DOI: 10.1097/00004872-200101000-00023     Document Type: Letter

References (11)

1. Effect of oral magnesium supplementation on blood pressure, platelet aggregation and calcium handling in deoxycorticosterone acetate-induced hypertension in rats
2. Effect of magnesium on calcium responses to vasopressin in vascular smooth muscle cells of spontaneously hypertensive rats
3. ++ concentrations in a subgroup of hypertensives. Membrane model for the pathogenesis of primary hypertension
4. ++ in erythrocytes of essential hypertension: Relation to blood pressure and serum divalent cations
5. ++ concentrations in smooth and striated muscle cells in spontaneously hypertensive rats
6. Importance of decreased intracellular phosphate and magnesium concentrations and reduced ATPase activities in spontaneously hypertensive rats
7. ++ intracellular concentrations in vascular smooth muscle cells from spontaneously hypertensive rats
8. ++ increase in response to pressure changes
9. Reduced intestinal epithelial cell brush border membrane calcium transport in spontaneously hypertensive rats
10. Calcium transport proteins, calcium absorption, and vitamin D
11. Membranous increased calcium and decreased magnesium concentrations in the pathogenesis of primary hypertension: A possible calcium magnesium antagonism