The effects of melatonin on Ca super(2+) homeostasis in endothelial cells

The effect of melatonin on the Ca super(2+) signaling process in bovine aortic endothelial cells (BAE) and in primary cultured vascular endothelial cells from normotensive Sprague Dawley (SDR) and genetically hypertensive (SHR) rats was investigated using the Ca super(2+) indicator Fura-2. Acute app...

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Bibliographic Details
Published in:Journal of pineal research 2002-08, Vol.33 (1), p.37-47
Main Authors: Pogan, L, Bissonnette, P, Parent, L, Sauve, R
Format: Article
Language:English
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Summary:The effect of melatonin on the Ca super(2+) signaling process in bovine aortic endothelial cells (BAE) and in primary cultured vascular endothelial cells from normotensive Sprague Dawley (SDR) and genetically hypertensive (SHR) rats was investigated using the Ca super(2+) indicator Fura-2. Acute applications of melatonin failed to initiate a Ca super(2+) response in the three cell types considered. However, preincubating SHR aortic endothelial cells with exposure to melatonin increased the internal Ca super(2+) release triggered by bradykinin (BK) and ATP while stimulating the related agonist-evoked Ca super(2+) entry. This effect appeared specific for SHR cells, as a similar incubation period failed to alter the Ca super(2+) responses in BAE and SDR cells. Because of the known overproduction of free radicals in SHR cells, the effect of melatonin on Ca super(2+) signaling was also tested in SDR and BAE cells exposed to the superoxide anion radical. Melatonin reversed the deleterious action of free radicals on Ca super(2+) signaling in both cases, suggesting that its stimulatory effect in SHR was linked to its antioxidative properties. Finally, experiments where melatonin was applied between successive BK stimulation periods showed an enhancement of the agonist-evoked Ca super(2+) entry in BAE and SDR cells. This effect appeared to be independent of the production of second messengers as no specific binding sites for melatonin, including MT1, MT2 and MT3 receptors, could be detected in BAE cells. We conclude that melatonin improves Ca super(2+) signaling in dysfunctional endothelial cells characterized by an overproduction of free radicals while stimulating the agonist-evoked Ca super(2+) entry in normal endothelial cells through a mechanism not related to its antioxidative properties.
ISSN:0742-3098