Robie N W
Am J Physiol. 1979 Sep;237(3):H326-31. doi: 10.1152/ajpheart.1979.237.3.H326.
Experiments were performed in anesthetized dogs to determine whether previously reported in vitro inhibition of sympathetic neurotransmitter release by acetylcholine could be demonstrated in the renal vasculature of the intact animal. Vasoconstrictor responses to renal sympathetic nerve stimulation at varying frequencies were compared to intra-arterial injections of norepinephrine before and during intra-arterial infusions of acetylcholine, 2.5--80 micrograms/min. The vasoconstrictor responses to nerve stimulation were inhibited to a greater extent than were responses to norepinephrine during infusions of acetylcholine. The inhibitory effects of acetylcholine on nerve stimulation were dose and frequency dependent. The inhibition was blocked by atropine but not altered by physostigmine. Changes in renal blood flow per se did not contribute to the inhibitory effect of acetylcholine, since another vasodilator agent, sodium acetate, did not affect the nerve stimulation-norepinephrine vasocontriction relationship. Thus, acetylcholine produced inhibition of in vivo renal sympathetic vasoconstrictor responses, and the receptor involved appears to be muscarinic.
在麻醉犬身上进行实验,以确定先前报道的乙酰胆碱在体外对交感神经递质释放的抑制作用在完整动物的肾血管系统中是否能够得到证实。在以2.5--80微克/分钟的速度动脉内输注乙酰胆碱之前和期间,将不同频率刺激肾交感神经时的血管收缩反应与动脉内注射去甲肾上腺素时的反应进行比较。在输注乙酰胆碱期间,对神经刺激的血管收缩反应比去甲肾上腺素的反应受到更大程度的抑制。乙酰胆碱对神经刺激的抑制作用呈剂量和频率依赖性。该抑制作用被阿托品阻断,但不受毒扁豆碱影响。肾血流量本身的变化对乙酰胆碱的抑制作用没有影响,因为另一种血管扩张剂醋酸钠并不影响神经刺激-去甲肾上腺素血管收缩关系。因此,乙酰胆碱可抑制体内肾交感神经血管收缩反应,且所涉及的受体似乎是毒蕈碱型的。