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.
","abstract_html":"<p>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 [Ca<sup>2+</sup>]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 Ca<sup>2+ </sup>than did magnesium-sufficient cells. Magnesium-deficient MNC of SHR accumulated more [Ca<sup>2+</sup>]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.</p>","abstract_has_math":false,"creators":["Gordon, Elaine Pringle"],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":"Chemistry and Biochemistry","degree_department":null,"school":null,"contributors":["Frank Lattanzio","Dieter Bartschat","Barbara Hargrave","Howard D. White"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1992,"date_issued":"1992-01-01T08:00:00Z","date_published":"1992-01-01T08:00:00Z","updated_at":"2026-07-24T03:35:08Z","subjects":["Hypertension","Magnesium","Calcium regulation","Cell Biology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://digitalcommons.odu.edu/biomedicalsciences_etds/102","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Frank Lattanzio","Dieter Bartschat","Barbara Hargrave","Howard D. 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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.
"]},{"key":"dc:title","label":"Title","values":["Magnesium Regulation of Calcium in Essential Hypertension"]}]}],"canonical_facts":{"dc:contributor":["Frank Lattanzio","Dieter Bartschat","Barbara Hargrave","Howard D. White"],"dc:creator":["Gordon, Elaine Pringle"],"dc:date.available":["2019-09-24T07:00:00Z"],"dc:description.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.
"],"dc:identifier":["https://digitalcommons.odu.edu/biomedicalsciences_etds/102"],"dc:subject":["Hypertension","Magnesium","Calcium regulation","Cell Biology"],"dc:title":["Magnesium Regulation of Calcium in Essential Hypertension"],"thesis:degree_discipline":["Chemistry and Biochemistry"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T03:35:08Z"}