Potter E K, McCloskey D I
Respir Physiol. 1979 Apr;36(3):367-73. doi: 10.1016/0034-5687(79)90048-3.
The changes in breathing accompanying increases in arterial pressure caused by intravenous injections of angiotensin II were examined in dogs anaesthetized with chloralose, and in unanaesthetized rabbits. They were compared with the effects on breathing caused when the alpha-adrenergic vasoconstrictor, phenylephrine, or inflation of an aortic balloon were used to raise blood pressure to comparable levels. Phenylephrine and balloon inflation always depressed breathing: this depression was secondary to the increase in arterial pressure and was abolished by denervation of the arterial baroreceptors. In every animal ventilation was greater with angiotensin II than it was at a comparable blood pressure achieved with phenylephrine or balloon inflation. When compared with control levels of ventilation, however, angiotensin II sometimes caused an increase in breathing, sometimes a reduction, and sometimes had little effect. When both carotid sinus and vagus nerves were cut, angiotensin II consistently stimulated breathing. This shows that angiotensin II has an independent stimulating effect on ventilation which cannot be attributed to inhibition of any baroreceptor-mediated respiratory restraint nor to stimulation of either arterial chemoreceptors or intrathoracic receptors which run to the CNS through the vagus.
在使用水合氯醛麻醉的犬以及未麻醉的兔中，研究了静脉注射血管紧张素II引起动脉压升高时伴随的呼吸变化。将这些变化与使用α-肾上腺素能血管收缩剂去氧肾上腺素或主动脉球囊充气使血压升高到可比水平时对呼吸的影响进行了比较。去氧肾上腺素和球囊充气总是会抑制呼吸：这种抑制是动脉压升高的继发结果，并且在切断动脉压力感受器的神经支配后会消失。在每只动物中，血管紧张素II引起的通气量都比使用去氧肾上腺素或球囊充气达到可比血压时更大。然而，与通气的对照水平相比，血管紧张素II有时会导致呼吸增加，有时会导致呼吸减少，有时影响不大。当切断双侧颈动脉窦和迷走神经时，血管紧张素II持续刺激呼吸。这表明血管紧张素II对通气有独立的刺激作用，这既不能归因于对任何压力感受器介导的呼吸抑制的抑制，也不能归因于对通过迷走神经传入中枢神经系统的动脉化学感受器或胸内感受器的刺激。
