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Beta-adrenergic-induced calcium efflux in rat parotid gland. Is mitochondrial Na+/Ca2+ exchange involved?

C Dreux1, C Huleux, D Eboué

  • 1Biochimie des transports cellulaires, CNRS URA 1116, Université Paris XI, Orsay, France.

Archives of Physiology and Biochemistry
|April 1, 1997
PubMed

Insights

Diltiazem inhibits mitochondrial calcium efflux in rat parotid glands, suggesting mitochondria may store calcium mobilized by beta-adrenergic stimulation. This drug affects calcium pools distinct from those targeted by carbachol.

Area of Science:

  • Cell Physiology
  • Pharmacology
  • Mitochondrial Function

Background:

  • Calcium (Ca2+) signaling is crucial for cellular processes, including secretion in exocrine glands like the parotid gland.
  • Mitochondria play a significant role in intracellular calcium homeostasis.
  • Diltiazem is a known calcium channel blocker, but its effects on mitochondrial calcium handling in exocrine glands require further elucidation.

Purpose of the Study:

  • To investigate the effects of diltiazem on calcium (Ca2+) efflux in rat parotid glands.
  • To determine if diltiazem influences mitochondrial calcium transport.
  • To explore the relationship between diltiazem, isoproterenol, and carbachol in modulating parotid gland calcium pools.

Main Methods:

  • Measurement of 45Ca efflux from isolated rat parotid glands and parotid lobules.
  • Assessment of mitochondrial Na+/Ca2+ exchange activity.
  • Evaluation of diltiazem's effects alone and in combination with isoproterenol and carbachol.

Main Results:

  • Diltiazem inhibited mitochondrial Na(+)-dependent calcium efflux in rat parotid glands.
  • Diltiazem did not affect calcium movements at the plasma membrane level.
  • Diltiazem induced 45Ca efflux from parotid lobules and acted on an intracellular calcium pool distinct from the IP3-sensitive one.

Conclusions:

  • Mitochondrial Na+/Ca2+ exchange is present and functional in rat parotid glands.
  • Diltiazem inhibits mitochondrial calcium efflux and may mobilize calcium from a non-IP3 sensitive intracellular pool.
  • These findings support the hypothesis that beta-adrenergic agonists (like isoproterenol) and muscarinic agonists (like carbachol) utilize different calcium pools, with mitochondria being a potential store for beta-adrenergic-stimulated calcium.

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