Physiological and pharmacological correlates of calcium antagonist receptors Academic Article uri icon


MeSH Major

  • Calcium
  • Calcium Channel Blockers
  • Heart
  • Receptors, Nicotinic
  • Synaptosomes


  • We studied voltage-sensitive and Na-dependent Ca2+ flux into synaptosomes as well as Na-dependent influx in cardiac sarcolemmal vesicles. Rapid, voltage-sensitive 45Ca2+ influx into synaptosomes is blocked by cadmium (IC50 1 microM) and the novel peptide toxin omega-conotoxin GVIA (30% of uptake blocked by 50 pM toxin), but not by dihydropyridine and phenylalkylamine calcium antagonists, even though [3H]dihydropyridines and [3H]phenylalkylamines bind to synaptosomes. The toxin also blocks voltage-sensitive neurotransmitter release from synaptosomes. Sodium-dependent Ca2+ flux into synaptosomes and cardiac sarcolemmal vesicles is inhibited by selected antihistamines, neuroleptics, and tricyclic antidepressants. We can elicit neurotransmitter release from synaptosomes by changing the Na gradient; this neurotransmitter release is absolutely Ca2+-dependent and blocked by Na+/Ca2+ exchange inhibitors, thereby suggesting that physiological neurotransmitter release may have a Na+/Ca2+ exchange component. More potent Na+/Ca2+ exchange inhibitors may have cardiovascular roles as inotropic agents or antagonists of calcium-related injury to cardiomyocytes during reperfusion or other disease states.

publication date

  • December 1987



  • Academic Article



  • eng

PubMed ID

  • 2455102

Additional Document Info

start page

  • S1

end page

  • 9


  • 10


  • SUPPL. 10