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High-affinity calcium binding in rat synaptosomal plasma membranes: decrease in young, genetically hypertensive rats.

A M Nunez, M A Devynck, P Meyer

    Journal of Neurochemistry
    |May 1, 1982
    PubMed
    Summary
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    Spontaneously hypertensive rats (SHR) show reduced calcium binding in brain synaptosomal plasma membranes compared to controls. This calcium binding abnormality may contribute to the development of genetic hypertension.

    Area of Science:

    • Neuroscience
    • Cardiovascular Physiology
    • Biochemistry

    Background:

    • Calcium ions are crucial for neurotransmitter release and neuronal function.
    • Altered calcium homeostasis is implicated in various cardiovascular diseases, including hypertension.
    • Synaptosomal plasma membranes are key sites for calcium regulation in neurons.

    Purpose of the Study:

    • To investigate calcium binding site characteristics in synaptosomal membrane fractions from spontaneously hypertensive rats (SHR) and normotensive controls.
    • To determine if differences in calcium binding exist between SHR and control rats at the nerve terminal level.
    • To explore the potential role of altered calcium binding in the pathogenesis of genetic hypertension.

    Main Methods:

    • Isolation of synaptosomal membrane fractions enriched in plasma membranes from rat brains.

    Related Experiment Videos

  • Characterization of high-affinity calcium binding sites using equilibrium binding assays.
  • Comparison of calcium binding capacity and affinity between SHR and normotensive control rats.
  • Assessment of calcium binding in the presence of the calcium ionophore A23187 to evaluate accessibility.

    • Main Results:

    • A large number of high-affinity calcium binding sites were identified in rat brain synaptosomal membranes.
    • No significant differences in whole synaptosomes were observed between SHR and control rats.
    • Plasma membrane-enriched fractions from SHR showed a 15-20% reduction in calcium binding capacity compared to controls.
    • The reduction in calcium binding in SHR was independent of calcium site accessibility, as confirmed by ionophore experiments.

    Conclusions:

    • Synaptosomal plasma membranes from SHR exhibit a reduced capacity for calcium binding.
    • This abnormality in neuronal calcium handling may be a contributing factor to the development of genetic hypertension.
    • The findings suggest a potential link between impaired calcium regulation at nerve endings and the pathophysiology of hypertension.