Date of Award

Winter 1992

Document Type


Degree Name

Doctor of Philosophy (PhD)


Chemistry and Biochemistry


Biomedical Sciences

Committee Director

Frank Lattanzio

Committee Member

Dieter Bartschat

Committee Member

Barbara Hargrave

Committee Member

Howard D. White


Essential hypertension is a complex disease which is treated by palliative methods, since the causal factors are as yet unknown. A variety of both genetic and environmental factors probably combine to produce chronic high blood pressure. A genetic model of essential hypertension, spontaneously hypertensive rats (SHR), and its control strain Wistar Kyoto (WKY) were used to investigate a possible environmental causal factor, cellular magnesium deficit, and its impact on the functional ability of the calcium ATPase. Rats were fed either a magnesium-deficient or a magnesium-sufficient diet for 10 weeks, after which the calcium ATPase activity was measured in intact red blood cells (RBC). Free intracellular calcium [Ca2+]i accumulation in response to a five minute 10 nM ionomycin challenge was estimated in blood mononuclear cells (MNC) loaded with the calcium indicator fura-2 AM. Plasma and RBC total magnesium were measured and found to be considerably lower in magnesium-deficient rats. Magnesium-deficient RBC of both SHR and WKY demonstrated lower Ca ATPase activity when stimulated either with 0.3 μΜ or 35 μΜ Ca2+ than did magnesium-sufficient cells. Magnesium-deficient MNC of SHR accumulated more [Ca2+]i than magnesium sufficient cells when challenged with ionomycin. However there was considerable individual variation. Results in WKY were not statistically different. These experiments showed that dietary magnesium can have a significant effect on the calcium handling of model cells and perhaps on the vascular smooth muscle cells of essential hypertensive patients, leading to increased vascular resistance.



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