Vascular Sympathetic Neurotransmission and Endothelial Dysfunction

Abstract

Endothelium is an important regulator of vascular tone via release of various endothelium- derived substances. Several studies have reported that endothelium may decrease the release of noradrenaline from vascular postganglionic sympathetic nerves and thus neuro- genic vasoconstriction. Endothelium derived-mediators (adenosine and NO) can modify vascular sympathetic neurotransmission and are relevant for vascular homeostasis. This is a relevant issue in terms of vascular homeostasis and, any modification, may lead to a deregulation process and to pathologies. Focus on NO-mediated effects on vascular sym- pathetic transmission will be done, discriminating the effects ascribed to NO generated by NO synthases located in the different vascular layers. A comparison between mesenteric/ tail arteries will also be explored, particularly the relevance of the transsynaptic modulation on noradrenaline release mediated by endothelial NO and adenosine in normotensive/ hypertensive vascular tissues. Adenosinergic system, namely adenosine, nucleoside transporters and adenosine receptors, can be influenced by endothelium mediators, namely by NO, causing alterations on the way these players interact with each other. In conditions where endothelium is compromised, a deregulation occurs with an increase in vascular sympathetic neurotransmission (as a consequence of adenosinergic system dynamic alter-ation). In summary, the impact of endothelial dysfunction on vascular neurotransmission is debated with particular focus on adenosinergic and nitroxidergic system dynamics.