Head G A, Elghozi J L, Korner P I
Baker Medical Research Institute, Prahran, Australia.
J Hypertens Suppl. 1988 Dec;6(4):S505-7. doi: 10.1097/00004872-198812040-00159.
We examined the cardiovascular responses to intracisternal administration of angiotensin II (Ang II) in conscious rabbits and determined the effects of removing baroreflex feedback inhibition. Administration of intracisternal bolus doses of Ang II produced short-duration dose-dependent increases in blood pressure (maximum response 30 mmHg) accompanied by bradycardia, with the dose required to produce the half maximal response averaging 5 pg. Dose-response curves to intracisternal Ang II spanned four log(dose) units from the threshold to the maximum doses (1-5 ng). After sino-aortic baroreceptor denervation the threshold for pressor responses was reduced by a factor of 1000, with the ED50 in these animals as low as 5 fg. No bradycardia was observed and the dose-pressor response curves were markedly steeper. The results suggest that in conscious rabbits Ang II receptors, presumably located in the brainstem, respond to minute intracisternal doses of Ang II. Furthermore, this site is normally inhibited by the input from arterial baroreceptors.
我们研究了清醒家兔对脑池内注射血管紧张素II（Ang II）的心血管反应，并确定了去除压力反射反馈抑制的影响。脑池内推注剂量的Ang II给药导致血压出现短期剂量依赖性升高（最大反应为30 mmHg），伴有心动过缓，产生半数最大反应所需的剂量平均为5 pg。脑池内Ang II的剂量-反应曲线从阈值到最大剂量（1-5 ng）跨越四个对数（剂量）单位。在去窦主动脉压力感受器后，升压反应的阈值降低了1000倍，这些动物的半数有效剂量（ED50）低至5 fg。未观察到心动过缓，剂量-升压反应曲线明显更陡。结果表明，在清醒家兔中，Ang II受体可能位于脑干，对脑池内微量的Ang II有反应。此外，该部位通常受到动脉压力感受器传入信号的抑制。
