Heart failure (HF) is associated with neurohumoral activation, which in turn leads to an increased peripheral resistance. In mesenteric vasculature, perivascular innervation plays relevant role maintaining vascular tonus and resistance. Therefore, we aimed to determine the possible alterations in superior mesenteric artery (SMA) perivascular innervation function in HF rats. HF was induced by coronary artery occlusion in male Wistar rats, and sham-operated (SO) rats were used as controls. After 12 weeks, a greater vasoconstrictor response to electrical field stimulation (EFS) was observed in endothelium-intact and -denuded SMA of HF rats. Alpha-adrenoceptor antagonist phentolamine diminished this response in a higher magnitude in HF than in SO animals. However, the noradrenaline (NA) reuptake inhibitor desipramine increased EFS-induced vasoconstriction more in segments from HF rats. Besides, EFS-induced NA release was greater in HF animals, due to a higher tyrosine hydroxylase expression and activity. P2 purinoceptor antagonist suramin reduced EFS-induced vasoconstriction only in segments from SO rats, and ATP release was lower in HF than in SO. Moreover, nitric oxide (NO) synthase inhibitor L-NAME enhanced EFS-induced vasoconstriction in a similar extent in both groups. HF was not associated with changes in EFS-induced NO release or the vasodilator response to NO donor sodium nitroprusside. In conclusion, HF post myocardial infarction enhanced noradrenergic function and diminished purinergic co-transmission in SMA and did not change nitrergic innervation. The net effect was an increased sympathetic participation on the EFS-induced vasoconstriction, that could help to understand the neurotransduction involved on the control of vascular tonus in HF.

中文翻译：

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在心力衰竭大鼠模型中肠系膜上动脉的交感神经转导增强：去甲肾上腺素和ATP的作用。

心力衰竭（HF）与神经体液激活有关，继而导致外周阻力增加。在肠系膜脉管系统中，血管周神经支配在维持血管紧张度和抵抗力方面起着重要作用。因此，我们旨在确定HF大鼠肠系膜上动脉（SMA）血管周围神经支配功能的可能改变。在雄性Wistar大鼠中，冠状动脉闭塞可诱发HF，以假手术（SO）大鼠为对照组。12周后，在HF大鼠的内皮完整和裸露的SMA中观察到对电场刺激（EFS）的更大的血管收缩反应。α-肾上腺素能受体拮抗剂酚妥拉明在HF中比在SO动物中更高程度地减弱了这种反应。然而，去甲肾上腺素（NA）再摄取抑制剂地昔帕明在HF大鼠的节段中增加了EFS诱导的血管收缩。此外，由于较高的酪氨酸羟化酶表达和活性，EFS诱导的HF动物的NA释放更大。P2嘌呤受体拮抗剂苏拉明仅在SO大鼠的节段中降低EFS诱导的血管收缩，并且HF中的ATP释放低于SO中的ATP释放。此外，两组中的一氧化氮（NO）合酶抑制剂L-NAME均以类似的程度增强了EFS诱导的血管收缩。HF与EFS诱导的NO释放变化或对NO供体硝普钠的血管舒张反应无关。总之，心肌梗死后的HF增强了SMA的去甲肾上腺素功能，并减少了嘌呤能的共同传递，并且没有改变神经能的神经支配。