Wellens D L, Snoeckx L H, De Wilde A M, Reneman R S
Arch Int Pharmacodyn Ther. 1975 May;215(1):20-30.
The influence of guanethidine on the nicotinic effects of acetylcholine was studied in anaesthetized atropinized dogs. Guanethidine (5 mg/kg i.v.) reversed the initial nicotinic pressor reaction, abolished the accompanying femoral vasoconstriction and reduced the increase of mean aortic flow. Therefore, nicotinic hypotension after guanethidine was due to a decrease of the peripheral vascular resistance. The height of the second pressor reaction was hardly affected by guanethidine. This drug inhibited the increases in mean aortic flow and heart rate but not the elevation of peripheral resistance, occurring at the secone nicotinic pressor phase. The present findings support the assumption that the initial hypertension is due to increased sympathetic outflow towards heart and vessels, whereas the second hypertension is due to adrenal medullary stimulation. The neurogenic femoral vasodilation at the onset of the second nicotinic pressor phase was blocked by guanethidine, which also inhibited the catecholamine-induced neurogenic vasodilation. These antagonisms may result from the interference of guanethidine with noradrenaline re-uptake.
在麻醉并用阿托品处理的犬中研究了胍乙啶对乙酰胆碱烟碱样作用的影响。静脉注射胍乙啶（5毫克/千克）可逆转最初的烟碱样升压反应，消除伴随的股血管收缩，并减少平均主动脉血流量的增加。因此，胍乙啶后的烟碱样低血压是由于外周血管阻力降低所致。第二次升压反应的高度几乎不受胍乙啶影响。该药物抑制了平均主动脉血流量和心率的增加，但不抑制在第二次烟碱样升压期出现的外周阻力升高。目前的研究结果支持这样的假设，即最初的高血压是由于交感神经向心脏和血管的输出增加，而第二次高血压是由于肾上腺髓质刺激。胍乙啶阻断了第二次烟碱样升压期开始时的神经源性股血管舒张，它也抑制了儿茶酚胺诱导的神经源性血管舒张。这些拮抗作用可能是由于胍乙啶干扰去甲肾上腺素再摄取所致。
