Potter Erica K, Tripovic Diana
Prince of Wales Medical Research Institute, Barker St, Randwick, Sydney, NSW, 2031, Australia.
Exp Brain Res. 2006 Aug;173(2):346-52. doi: 10.1007/s00221-006-0550-3. Epub 2006 May 30.
We have investigated the effect of the Y2 receptor agonist (Y2 agonist; N-acetyl [Leu28,31] NPY 24-36), on contractions evoked by transmural electrical stimulation of sympathetic nerves of isolated arteries from a range of vascular beds in rats and guinea pigs. Contractions evoked by transmural stimulation of the rat renal, mesenteric and femoral arteries were significantly attenuated in the presence of the Y2 agonist. In these arteries, contractions were significantly inhibited in the presence of an alpha-adrenoceptor antagonist (76-97%). So we conclude that these responses were primarily mediated by noradrenaline and that the Y2 agonist attenuates the release of noradrenaline via presynaptic Y2 receptors. Contractions of the rat carotid artery were not attenuated by the Y2 agonist but were completely abolished in the presence of an alpha-adrenoceptor antagonist suggesting that in this artery the Y2 agonist has no effect on release of noradrenaline. In the guinea pig, carotid arteries contractions evoked by transmural nerve stimulation were attenuated in the presence of the Y2 agonist and inhibited by an alpha-adrenoceptor antagonist 75-87% suggesting that the Y2 agonist attenuates the release of noradrenaline via presynaptic Y2 receptors in this vessel. In the guinea pig femoral artery contractions evoked by transmural stimulation were not modified in the presence of the Y2 agonist but were completely abolished in the presence of an alpha-adrenoceptor antagonist. This suggests that the Y2 agonist does not modify noradrenaline release in this vessel. Contractions of the guinea pig mesenteric artery were significantly potentiated by the Y2 agonist, possibly by potentiation of neuropeptide Y (NPY) at the Y1 receptor. The Y1 antagonist inhibited more than 70 % of the response, indicating that the majority of the contraction was mediated by NPY. The current study demonstrates heterogeneity of neurotransmitter substances in sympathetic nerves supplying vascular beds within and across species and in subsequent functional response.
我们研究了Y2受体激动剂（Y2激动剂；N-乙酰基[Leu28,31]神经肽Y 24-36）对大鼠和豚鼠一系列血管床分离动脉交感神经经壁电刺激诱发的收缩的影响。在Y2激动剂存在的情况下，大鼠肾动脉、肠系膜动脉和股动脉经壁刺激诱发的收缩明显减弱。在这些动脉中，α-肾上腺素能受体拮抗剂存在时收缩明显受到抑制（76-97%）。因此我们得出结论，这些反应主要由去甲肾上腺素介导，并且Y2激动剂通过突触前Y2受体减弱去甲肾上腺素的释放。大鼠颈动脉的收缩未被Y2激动剂减弱，但在α-肾上腺素能受体拮抗剂存在时完全被消除，这表明在该动脉中Y2激动剂对去甲肾上腺素的释放没有影响。在豚鼠中，经壁神经刺激诱发的颈动脉收缩在Y2激动剂存在时减弱，在α-肾上腺素能受体拮抗剂存在时受到75-87%的抑制，这表明Y2激动剂通过该血管中的突触前Y2受体减弱去甲肾上腺素的释放。在豚鼠股动脉中，经壁刺激诱发的收缩在Y2激动剂存在时未改变，但在α-肾上腺素能受体拮抗剂存在时完全被消除。这表明Y2激动剂在该血管中不改变去甲肾上腺素的释放。豚鼠肠系膜动脉的收缩被Y2激动剂显著增强，可能是通过Y1受体处神经肽Y（NPY）的增强作用。Y1拮抗剂抑制了超过70%的反应，表明大部分收缩由NPY介导。当前研究证明了在不同物种内和跨物种供应血管床的交感神经中神经递质物质的异质性以及随后的功能反应。
