von Kügelgen I, Starke K
J Physiol. 1985 Oct;367:435-55. doi: 10.1113/jphysiol.1985.sp015834.
The largest rami caecales of the ileocolic artery, which is a branch of the mesenteric artery, were perfused at a constant rate of flow. Either vasoconstriction (as an increase in perfusion pressure) or the release of previously incorporated [3H]-noradrenaline was measured. Noradrenaline and ATP, but not carbachol, serotonin, adenosine, Arg-vasopressin and neuropeptide Y, caused marked vasoconstriction. When the sympathetic vasoconstrictor axons in the arterial wall were stimulated by electrical field pulses (either 5 pulses at 10 Hz or 100 pulses at 5 Hz; 0.3 ms pulse width, 200 mA current strength), the ensuing vasoconstriction was at best slightly reduced by phentolamine, prazosin and phenoxybenzamine. The response to 100 pulses, 5 Hz was even enhanced by phentolamine and yohimbine. All antagonists except yohimbine blocked the effect of exogenous noradrenaline. Prazosin did not change the effect of exogenous ATP. alpha,beta-Methylene-ATP (3-15 mumol/l) elicited transient vasoconstriction. Subsequently, responses to ATP as well as to electrical stimulation were reduced and recovered slowly. The response to noradrenaline was not changed. That part of the electrically induced vasoconstriction that remained after alpha,beta-methylene-ATP was almost abolished by phentolamine or prazosin. Pre-treatment of the animals with reserpine decreased but did not prevent the electrically evoked contraction of their arteries. The reserpine-resistant response was not changed by prazosin but was abolished by alpha,beta-methylene-ATP. The vasoconstriction elicited by electrical pulses was not affected by atropine or methysergide but was entirely blocked by tetrodotoxin, guanethidine or exposure to 6-hydroxydopamine. In arteries pre-incubated with [3H]-noradrenaline, electrical stimulation (100 pulses at 5 Hz) increased the outflow of tritium. The evoked overflow was blocked by tetrodotoxin, not changed by alpha,beta-methylene-ATP (9 mumol/l) or prazosin, and enhanced by phentolamine, phenoxybenzamine and yohimbine. We conclude that, in the branch of the mesenteric artery examined, both noradrenaline and ATP or a closely related compound transmit information from sympathetic neurones to smooth muscle. An alpha-adrenoceptor antagonist can reduce neurogenic vasoconstriction by blockade of post-junctional alpha-(probably alpha 1) receptors, reserpine by selective depletion of noradrenaline, and alpha,beta-methylene-ATP by desensitization of the post-junctional ATP (probably P2) receptor mechanism. Noradrenaline and ATP appear to be released from the same neurone. In addition, prejunctional alpha 2-adrenergic autoinhibition of transmitter release operates in the artery. alp
肠系膜动脉分支回结肠动脉的最大盲肠支以恒定流速灌注。测量血管收缩（表现为灌注压力升高）或先前掺入的[3H] - 去甲肾上腺素的释放。去甲肾上腺素和ATP可引起明显的血管收缩，而卡巴胆碱、5 - 羟色胺、腺苷、精氨酸加压素和神经肽Y则无此作用。当通过电场脉冲刺激动脉壁中的交感缩血管轴突（10Hz的5个脉冲或5Hz的100个脉冲；脉冲宽度0.3ms，电流强度200mA）时，酚妥拉明、哌唑嗪和酚苄明至多只能轻微减弱随后出现的血管收缩。酚妥拉明和育亨宾甚至增强了对100个脉冲（5Hz）的反应。除育亨宾外，所有拮抗剂均能阻断外源性去甲肾上腺素的作用。哌唑嗪不改变外源性ATP的作用。α,β - 亚甲基ATP（3 - 15μmol/L）引起短暂的血管收缩。随后，对ATP以及电刺激的反应减弱且恢复缓慢。对去甲肾上腺素的反应未改变。α,β - 亚甲基ATP处理后，电诱导的血管收缩中剩余的部分几乎被酚妥拉明或哌唑嗪消除。用利血平预处理动物可减少但不能阻止其动脉的电诱发收缩。利血平抵抗性反应不受哌唑嗪影响，但被α,β - 亚甲基ATP消除。电脉冲引起的血管收缩不受阿托品或麦角新碱影响，但完全被河豚毒素、胍乙啶或暴露于6 - 羟基多巴胺阻断。在预先用[3H] - 去甲肾上腺素孵育的动脉中，电刺激（5Hz的100个脉冲）增加了氚的流出。诱发的溢出被河豚毒素阻断，不受α,β - 亚甲基ATP（9μmol/L）或哌唑嗪影响，而被酚妥拉明、酚苄明和育亨宾增强。我们得出结论，在所检查的肠系膜动脉分支中，去甲肾上腺素和ATP或一种密切相关的化合物都将信息从交感神经元传递至平滑肌。α - 肾上腺素能拮抗剂可通过阻断节后α - （可能是α1）受体来减少神经源性血管收缩，利血平通过选择性耗竭去甲肾上腺素，α,β - 亚甲基ATP通过使节后ATP（可能是P2）受体机制脱敏。去甲肾上腺素和ATP似乎从同一神经元释放。此外，动脉中存在递质释放的节前α2 - 肾上腺素能自身抑制作用。
