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Platelet abnormalities and the pathophysiology of essential hypertension

Experientia volume 44, pages 94–97 (1988)Cite this article

Summary

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.

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Affiliations

  1. Departments of Research and Medicine, University Hospital, CH-4031, Basel, (Switzerland)

    F. R. Bühler & T. J. Resink

Authors
  1. F. R. Bühler
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  2. T. J. Resink
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Bühler, F.R., Resink, T.J. Platelet abnormalities and the pathophysiology of essential hypertension. Experientia 44, 94–97 (1988). https://doi.org/10.1007/BF01952187

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  • DOI: https://doi.org/10.1007/BF01952187

Key words

  • Platelets
  • intracellular calcium concentration
  • essential hypertension
  • cyclic nucleotides