dinoprost and Magnesium-Deficiency

Wistar rats were fed a low magnesium diet for 8 or 12 weeks, resulting in reduced levels of magnesium in plasma, heart, and skeletal muscle, as compared with pair-fed control rats. The magnesium-deficient rats also had reduced tissue levels of potassium. Coronary arteries and thoracic aorta from magnesium-deficient rats and control rats were incubated in tissue baths and the contractile responses to potassium, 5-hydroxy-tryptamine, and prostaglandin F2 alpha were investigated using a sensitive in vitro system. The concentration-contraction curve, for all agents was shifted to the left in coronary arteries from magnesium-deficient rats. In aorta from magnesium-deficient rats, the pattern of change in reactivity to these agonists was not uniform: the concentration-contraction curve for 5-hydroxytryptamine was shifted to the left, the contractile response to prostaglandin F2 alpha was reduced, while there was no change in the response to potassium. The contractile response to the administration of calcium to calcium-depleted, potassium-depolarized vessels from magnesium-deficient rats was enhanced; the effect was more pronounced in coronary arteries as compared to the aorta. Hence, the vasomotor reactivity of coronary arteries appears to be more sensitive than is the aorta during magnesium-deficient conditions.

Topics: Animals; Aorta; Coronary Vessels; Dinoprost; In Vitro Techniques; Magnesium Deficiency; Male; Potassium; Rats; Rats, Inbred Strains; Serotonin; Vasoconstriction

Plasma and tissue concentrations of prostanoids PGE2, PGF2 alpha. 6-keto-PGF1 alpha (a stable metabolite of prostacyclin) and TXB2 (a stable metabolite of thromboxane A2) were measured in normal and magnesium-deficient rats. The mean values for prostanoids in plasma were significantly higher in magnesium-deficient rats than in normals (515 +/- 43 vs 296 +/- 31 pg/ml for 6-keto-PGF1 alpha, p less than 0.01, 3700 +/- 322 vs 346 +/- 33 pg/ml for TXB2, p less than 0.001 and 1234 +/- 132 vs 434 +/- 51 pg/ml for PGE2, p less than 0.001). Tissue levels of prostanoids were also significantly higher in magnesium-deficient rats as compared to normals. The increased synthesis of prostanoids is apparently linked to enhanced influx and translocation of Ca++ into the cells. If the adenylate cyclase is inhibited in magnesium deficiency, the lowered c-AMP will permit a high cyclooxygenase activity and a drastic increase in TXB2. It is possible that the changes in prostaglandin synthesis in magnesium deficiency are linked to the development of different diseases.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Arachidonic Acid; Arachidonic Acids; Calcium; Cyclic AMP; Dinoprost; Dinoprostone; Female; Magnesium Deficiency; Prostaglandins; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains; Thromboxane B2; Thymus Gland