title: Platelet abnormalities and the pathophysiology of essential hypertension.
abstract: The mechanisms whereby intracellular calcium concentration is controlled are briefly reviewed. With the current knowledge of both calcium homeostasis and the function and properties of cellular Ca2+-target proteins/signal transduction systems, a dysfunction of cellular calcium metabolism is considered in relation to the pathogenesis of hypertension. Although the enhanced peripheral vascular resistance characteristic of hypertension is ultimately a function of Ca2+ availability for smooth muscle cell contraction, the platelet possesses many parallel biochemical and physiological properties. Therefore, we have utilized the platelet as the cell-model for investigating the role of Ca2+ in hypertension disorders. An overview of Ca2+-linked platelet processes altered in essential hypertension is presented, and an attempt is made to integrate these multiple aberrations in a fundamental membrane lesion.
authors.affiliation: Department of Research, University Hospital, Basel, Switzerland.
authors.forename: F R
authors.initials: FR
authors.lastname: Bühler
authors.forename: T J
authors.initials: TJ
authors.lastname: Resink
mesh_terms: D001792:Blood Platelets / Q000502:physiology*; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D003600:Cytosol / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000378:metabolism / Q000473:pathology; D009712:Nucleotides, Cyclic / Q000378:metabolism; D009994:Osmolar Concentration; D010716:Phosphatidylinositols / Q000378:metabolism
chemical_list: D002135:Calcium-Binding Proteins; D009712:Nucleotides, Cyclic; D010716:Phosphatidylinositols; D002118:Calcium