Ionic mechanisms involved in the secretory effects of histamine in the rat adrenal medulla

Histamine activation of H1 receptors elicited the release of adrenaline from in vitro perfused rat adrenal with an EC50 of 3 microM. Neither Na+ deprivation nor complete membrane depolarization abolished the histamine-mediated secretory response but it was partially dependent on extracellular Ca2+. Nitrendipine and BAY-K-8644 affected the release induced by histamine concentrations at over 3 microM. Delayed application of histamine pulses, after external Ca2+ removal, led to a decline in to a plateau at 50% of the initial release. Pretreatment with ionomycin abolished this Ca2+ deprivation-resistant component. These data suggest that secretion evoked by low concentrations of histamine occurs by mobilization of Ca2+ from internal stores whereas higher concentrations use Ca2+ from both intracellular and extracellular sources.