Basal forebrain neurons control intracortical arterioles by releasing acetylcholine (Ach), which stimulates endothelial cells (ECs) to produce the vasodilating gasotransmitter, nitric oxide (NO). Surprisingly, the mechanism by which Ach induces NO synthesis in brain ECs is still unknown. An increase in intracellular Ca2+ concentration ([Ca2+]i) recruits a multitude of endothelial Ca2+-dependent pathways, such as Ca2+/calmodulin endothelial NO synthase (eNOS). The present investigation sought to investigate the role of intracellular Ca2+ signaling in Ach-induced NO production in bEnd5 cells, an established model of mouse brain microvascular ECs
Acetylcholine induces nitric oxide production by inducing intracellular Ca2+ oscillations in mouse brain endothelial cells
ZUCCOLO, ESTELLA;D'ANGELO, EGIDIO UGO;MOCCIA, FRANCESCO
2015-01-01
Abstract
Basal forebrain neurons control intracortical arterioles by releasing acetylcholine (Ach), which stimulates endothelial cells (ECs) to produce the vasodilating gasotransmitter, nitric oxide (NO). Surprisingly, the mechanism by which Ach induces NO synthesis in brain ECs is still unknown. An increase in intracellular Ca2+ concentration ([Ca2+]i) recruits a multitude of endothelial Ca2+-dependent pathways, such as Ca2+/calmodulin endothelial NO synthase (eNOS). The present investigation sought to investigate the role of intracellular Ca2+ signaling in Ach-induced NO production in bEnd5 cells, an established model of mouse brain microvascular ECsI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
