Revista chilena de historia natural
versión impresa ISSN 0716-078X
LUXORO, MARIO y VINET, RAUL. Physiological bases for an interaction between chromaffin and endothelial cells from the adrenal gland. Rev. chil. hist. nat. [online]. 2001, vol.74, n.1, pp. 39-45. ISSN 0716-078X. http://dx.doi.org/10.4067/S0716-078X2001000000009.
In this work we investigated the possible interactions between the endothelial cells from the adrenal gland and the substances related with the secretion from the chromaffin cells. In order to do so, we studied the effect of acetyl-choline (ACh) or of catecholamines (CA) on the level of the membrane potential and the cytoplasmic concentration of free calcium ([Ca2+]i) in the endothelial cells. Our results show that ACh as well as nicotine, but not muscarine, are able to induce an increase in [Ca2+]i and membrane depolarization of the endothelial cells. The nicotinic antagonist, hexamethonium, inhibits both the action of nicotine and of ACh, which suggests the presence of nicotinic receptors. On the other hand, CA (adrenaline as much as noradrenaline or a1-adrenergic agonists) also produce a rise in [Ca2+]i in endothelial cells but not a clear depolarization. In this case, the increase is biphasic, being the first phase a very rapid peak, independent of the external Ca2+ while the second phase shows oscillations and depends on the extracellular Ca2+. This phase is diminished if the calcium channels are blocked. Since it has been demonstrated that an increment of [Ca2+]i in endothelial cells triggers the secretion of vasodilator substances such as prostacyclin and nitric oxide, we propose that this might be a compensatory mechanism in order to compensate the enormous vasoconstrictor effect that the secreted CA should have
Palabras llave : endothelial; chromaffin; receptors; interactions.