Weber M A, Drayer J I, Purdy R E, Frankfort P P, Ricci B A
Life Sci. 1985 May 20;36(20):1897-907. doi: 10.1016/0024-3205(85)90438-2.
The pressor interactions between angiotensin II and norepinephrine were investigated in conscious New Zealand white rabbits receiving a low sodium diet. Angiotensin II was administered continuously by intraperitoneal osmotic pumps in a subpressor dose so as to avoid the potentially confounding effects of experimentally-induced hypertension. Norepinephrine challenges were given as a series of graded intravenous boluses. During the 3 days of study the baseline blood pressure in the angiotensin-treated rabbits (n=10) did not differ from that in controls (n=10) whose intraperitoneal pumps contained only diluent. After 24 hours the systolic and diastolic blood pressure responses to norepinephrine in the angiotensin-treated group were, on average, 45% and 30% higher than in the controls; after 72 hours, they were 46% and 34% higher. Although the pressor amplitudes were increased by angiotensin II, they were not prolonged. Thus, facilitation by the subpressor angiotensin II of the blood pressure responses to norepinephrine did not seem dependent upon alterations in endogenous sympathetic mechanisms or the uptake of norepinephrine; nor could it be explained by sodium retention. It is possible that angiotensin II exhibits its effect by enhancing contractile responsiveness to norepinephrine at the postreceptor level.
在接受低钠饮食的清醒新西兰白兔中，研究了血管紧张素II与去甲肾上腺素之间的升压相互作用。血管紧张素II通过腹腔内渗透泵以低于升压剂量持续给药，以避免实验性高血压可能产生的混淆效应。去甲肾上腺素激发以一系列分级静脉推注的形式进行。在研究的3天中，接受血管紧张素治疗的兔子（n = 10）的基线血压与腹腔泵仅含稀释剂的对照组（n = 10）的基线血压没有差异。24小时后，血管紧张素治疗组对去甲肾上腺素的收缩压和舒张压反应平均比对照组高45%和30%；72小时后，分别高46%和34%。虽然血管紧张素II增加了升压幅度，但并未延长升压时间。因此，低于升压剂量的血管紧张素II对去甲肾上腺素血压反应的促进作用似乎不依赖于内源性交感神经机制的改变或去甲肾上腺素的摄取；也不能用钠潴留来解释。血管紧张素II可能通过在受体后水平增强对去甲肾上腺素的收缩反应性来发挥其作用。
