Date of Award

Winter 1992

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Chemistry and Biochemistry

Program/Concentration

Biomedical Sciences

Committee Director

Frank Lattanzio

Committee Member

Dieter Bartschat

Committee Member

Barbara Hargrave

Committee Member

Howard D. White

Abstract

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.

DOI

10.25777/crae-6z57

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