M. Frey
University of Freiburg
29 Papers
524 Citations
M. Frey is an academic researcher from University of Freiburg. The author has contributed to research in topics: Calcium & Arteriosclerosis. The author has an hindex of 14, co-authored 29 publications.
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Papers
Antihypertensive and arterial anticalcinotic effects of calcium antagonists
TL;DR: In physiologic experiments, calcium antagonists normalize the blood pressure of spontaneously hypertensive rats, neutralize various vasoconstrictor agents, and greatly reduce the sensitivity of the systemic arteries and arterioles to mechanical stimuli, which can produce additional vasconstriction, if a rise in intraluminal pressure stretches the vascular wall (Bayliss effect).
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The role of calcium in the pathogenesis of experimental arteriosclerosis
TL;DR: It is predicted that in future a more comprehensive theory of arteriosclerosis should take into account disorders of both lipid and calcium metabolism.
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Consequences of uncontrolled calcium entry and its prevention with calcium antagonists
TL;DR: Intracellular Ca2+ overload proved to the common denominator in the pathogenesis of severe myocardial fibre injury and death produced under the following circumstances: Overdoses of beta-adrenergic catecholamines, dihydrotachysterol or vitamin D3, alimentary K+ or Mg2+ deficiency, hereditary cardiomyopathy of Syrian hamsters.
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Experimental vasoprotection by calcium antagonists against calcium-mediated arteriosclerotic alterations.
TL;DR: Data indicate that various Ca-consuming processes demand a progressive uptake of Ca into arterial walls if Ca-dominated types of arteriosclerosis develop, and specific Ca antagonists inhibit Ca-mediated arteriosclerotic alterations by preventing progressive mural Ca incorporation.
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Experimental basis of the long-term therapy of arterial hypertension with calcium antagonists
TL;DR: An important effect of Ca++ antagonists that is demonstrated in experiments on SHRs is the prevention of progressive arterial Ca++ overload, which otherwise produces severe calcinotic or arteriosclerotic damage of the arterial walls, and arterial integrity can be totally preserved.
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