GARDIER R W, JAMES E A, JOHNSON P C, RICHARDS A B, ROESCH R P
Br J Pharmacol Chemother. 1963 Jun;20(3):579-85. doi: 10.1111/j.1476-5381.1963.tb01495.x.
The pressor response to acetylcholine in the atropinized dog resulted from an increase in cardiac output. The pressor response was attributed solely to the release of adrenaline from the adrenal medulla. After giving compound P-286 (N-diethylaminoethyl-N-isopentyl-N'N'-di-isopropylurea) to these dogs, acetylcholine lowered blood pressure, owing to a decrease in total peripheral resistance in the absence of an increase in cardiac output. P-286 presumably blocked the liberation of adrenaline from the adrenal glands by acetylcholine. The blood vessels contributing to the fall in peripheral resistance were not in the intestines. The fall in blood pressure was not blocked by dichloroisoprenaline and it was still present in dogs treated with reserpine. It is suggested that the fall in blood pressure was due to stimulation of ganglion cells subserving vasodilatation.
在给予阿托品的犬中，对乙酰胆碱的升压反应是由于心输出量增加所致。该升压反应完全归因于肾上腺髓质释放肾上腺素。给这些犬注射化合物P - 286（N - 二乙氨基乙基 - N - 异戊基 - N'N' - 二异丙基脲）后，乙酰胆碱使血压降低，这是因为在没有心输出量增加的情况下总外周阻力降低。P - 286可能阻断了乙酰胆碱从肾上腺释放肾上腺素。导致外周阻力下降的血管不在肠道。血压下降未被二氯异丙肾上腺素阻断，并且在用利血平治疗的犬中仍然存在。提示血压下降是由于支配血管舒张的神经节细胞受到刺激所致。
