Rettig R, Healy D P, Printz M P
Brain Res. 1986 Feb 5;364(2):233-40. doi: 10.1016/0006-8993(86)90835-8.
The role of the angiotensin II system within the nucleus tractus solitarii (NTS) in central cardiovascular control was investigated by local microinjections of angiotensin II and the angiotensin II receptor antagonist saralasin. Microinjections of 1 ng angiotensin II into the NTS resulted in a monophasic depressor response (-7.3 +/- 1.7 mm Hg), while higher doses were characterized by a biphasic response, with an initial decrease followed by a subsequent increase in blood pressure (10 ng: -4.7 +/- 1.3/+7.9 +/- 1.1 and 100 ng: -2.4 +/- 1.2/+7.5 +/- 1.2 mm Hg). Heart rate decreased significantly following microinjections of 1 and 10 ng angiotensin II (-27 +/- 5.0 and -15 +/- 5.9 bpm), while with 100 ng angiotensin II there was no significant effect on heart rate. Prior i.v. administration of atropine (1 mg/kg) abolished the bradycardia, but did not significantly affect the blood pressure response. Microinjections of saralasin into the NTS elicited a dose-dependent pressor response (10 ng: 6.0 +/- 1.5 mm Hg; 100 ng: 16.8 +/- 3.4 mm Hg) and tachycardia (10 ng: 5 +/- 3.2 bpm; 100 ng: 17 +/- 4.4 bpm). Our data support the hypothesis that angiotensin II acts on specific receptors within the NTS to modulate peripheral cardiovascular responses. The cardiovascular effects elicited by microinjections of the peptide exhibit complicated dose-response relationships. The effects on heart rate, but not on blood pressure, appear to be mediated by parasympathetic activation.
通过向孤束核（NTS）局部微量注射血管紧张素II和血管紧张素II受体拮抗剂沙拉新，研究了孤束核内血管紧张素II系统在中枢心血管控制中的作用。向孤束核微量注射1 ng血管紧张素II会导致单相降压反应（-7.3±1.7 mmHg），而较高剂量则表现为双相反应，最初血压下降，随后血压升高（10 ng：-4.7±1.3/+7.9±1.1；100 ng：-2.4±1.2/+7.5±1.2 mmHg）。微量注射1 ng和10 ng血管紧张素II后心率显著下降（-27±5.0和-15±5.9次/分钟），而注射100 ng血管紧张素II对心率无显著影响。预先静脉注射阿托品（1 mg/kg）可消除心动过缓，但对血压反应无显著影响。向孤束核微量注射沙拉新会引发剂量依赖性升压反应（10 ng：6.0±1.5 mmHg；100 ng：16.8±3.4 mmHg）和心动过速（10 ng：5±3.2次/分钟；100 ng：17±4.4次/分钟）。我们的数据支持以下假设：血管紧张素II作用于孤束核内的特定受体，以调节外周心血管反应。微量注射该肽所引发的心血管效应呈现复杂的剂量反应关系。对心率而非血压的影响似乎是由副交感神经激活介导的。
