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Furthermore, in the cardiovascular system, NO can also interplay with the adrenergic pathway. NO source is, most probably, endothelial since noradrenaline release in the presence of a β-adrenoceptor agonist, isoprenaline (300 nM), caused an increase of noradrenaline release (175.10 13.8%, n = 11), but the increase observed was lower in endothelium-denuded arteries (129.92 13.1%, n = 7). Therefore, these data support the possibility, previously raised by Balligand et al. [86] and by Conti et al. [87], that NO production can lead to an increase in noradrenaline release, as a consequence of adrenergic receptors activation, namely of facilita-

P < 0.05 (ANOVA followed by post-hoc Holm-Sidak's multicomparisons t-test).

Figure 4. Influence of adenosine A1 receptor antagonist (DPCPX, 100 nM) and adenosine A2A receptor antagonist (SCH 58261, 20 nM), adenosine kinase inhibitor (ITU, 100 nM) and nucleoside transporter inhibitor (NBTI, 5 μM) in the effect elicited by a nitric oxide donor, DEA-NONOate (10 μM) on the electrically evoked tritium overflow, in mesenteric and tail arteries. Values are mean SEM from 4 to 12 artery segments. Significant differences from DEA-NONOate effect alone: \*

In addition to the direct effects exerted by several substances on smooth muscle cells, which can cause vasodilation or vasoconstriction, the evidence that endothelium-derived factors can also influence sympathetic neurotransmission that reinforces the importance of endothelium and of its putative role in pathologies. Indeed, vascular sympathetic neurotransmission and the interplay exerted by endothelium-derived substances are, therefore, relevant in the homeostasis of vascular tone. In pathophysiological conditions, especially when endothelium is injured, their impact on neurotransmission account, at least in part, for the occurring vasoconstriction.

tory β-adrenoceptors.

P < 0.05 and from mesenteric artery: #

338 Endothelial Dysfunction - Old Concepts and New Challenges

4. Current and future developments

Joana Sousa1,2 and Carmen Diniz1,2\*

\*Address all correspondence to: cdiniz@ff.up.pt

1 LAQV/REQUIMTE, Faculty of Pharmacy, University of Porto, Portugal

2 Laboratory of Pharmacology, Department of Drug Science, Faculty of Pharmacy, University of Porto, Portugal
