Cotransmission from sympathetic vasoconstrictor neurons: differences in guinea-pig mesenteric artery and vein

Endothelin (ET)-1-Induced Inhibition of ATP Release from PC-12 Cells Is Mediated by the ETBReceptor: Differential Response to ET-1 on ATP, Neuropeptide Y, and Dopamine Levels

“…At lower frequencies of stimulation, ATP levels reached a peak at 20 s, after which levels diminished with continued stimulation; however, peak levels of NE were not observed until 40 s and remained constant during the period of stimulation (Todorov et al, 1994). In contrast, NPY release from sympathetic nerves required higher frequencies of stimulation, which can be inhibited by the NPY Y 1 -specific antagonist BIBP3226 (Smyth et al, 2000).…”

Purinergic receptors in the splanchnic circulation

“…It is a well known fact that sympathetic neurons release both noradrenaline and ATP, which function as co-transmitters [156,157]. Examples of this adrenergic-purinergic cotransmission have also been observed in splanchnic vascular tissues such as mesenteric artery [181], mesenteric vein [155] and hepatic artery [12]. Activation of adenosine A 1 receptors by exogenous applied adenosine or its analogues has been shown to inhibit the release of both adrenergic and purinergic transmitters [38].…”

“…This has led to the conclusion that ATP is not involved in these junctional events [65,67] and, hence, is not released during nerve stimulation. However, a study on guinea-pig mesenteric vessels [155] revealed that arterial contractile response to sympathetic nerve stimulation is due exclusively to noradrenaline, whereas at least three different neurotransmitters (noradrenaline, ATP and neuropeptide Y) appear to contribute to the venous neural response. In another study, electric field stimulation induced ATP overflow in the guinea-pig mesenteric vein [8].…”

“…The difference in the contribution of ATP to the neural response in artery and vein was suggested to be related to the presence of different populations of ATP receptors, i.e., in artery, rapidly desensitizing P2X 1 receptors predominate whereas in vein, non-desensitizing P2Y receptors predominate [116]. However, the apparent contradictory results between these different studies [67,82,155] may also be ascribed to differences in the methodological approaches (evaluation of membrane potentials by electrophysiology vs contractile and [ 3 H]-noradrenaline release studies) or to the size of the vessels studied (the studies of Kreulen [82] involved a broader range of internal diameters of the vessels). Besides, there might be differences in the postjunctional effects of prejunctionally released neurotransmitters, as it is suggested to occur in the human saphenous vein [147], where ATP is co-released with noradrenaline but did not appear to generate the non-adrenergic component of contraction.…”

Properties of the Venous and Arterial Innervation in the Mesentery.

“…The differences in the slow depolarizations evoked by sympathetic nerve stimulation may also be accounted for by differences in the receptor populations of artery and vein. The slow depolarization of arterial smooth muscle is mediated mostly by norepinephrine acting on postjunctional alpha-1 receptors, whereas the depolarization of venous smooth muscle is mediated by a combination of alpha-1, alpha-2, and NPY receptors (Eckman et al, 1988;Smyth et al, 2000). The confluence of these multiple constricting influences may account for the proportionately greater venous depolarization and contraction in response to low frequency nerve stimulation.…”