The octapeptide, angiotensin II (AII), is made from the relatively inactive angiotensin I (AI) by the action of angiotensin converting enzyme (ACE) in the pulmonary circulation. AII is one of the strongest vasopressor agents and has been investigated for many years as a cause of essential hypertension.
The present investigation showed the effects of AII on the contraction of rabbit pulmonary artery and aorta with various vasoconstrictors.
Male rabbits weighing 2.7-3.0kg were killed, the pulmonary artery and the descending aorta were removed and suspended in a bioassay glass chamber superfused with Krebs-Hensleit solution at 37°C saturated with oxygen and carbon dioxide (95: 5, v/v).
Tissue contraction was detected by an isotonic transducer (ME Commercial, Tokyo, Japan) and recorded using a polyrecorder.
1) Rabbit aorta strip showed a bigger contraction than the rabbit pulmonary artery strip with the same dose of AII.
2) The effects of various vasoconstrictor agents on the rabbit pulmonary artery and the descending aorta strip were remarkably increased with continuous infusion of a low dose of AII (0.5ng/ml).
3) These results suggest that AII by itself acts on the vascular smooth muscle directly as a vasoconstrictor agent and that AII also acts on the vascular smooth muscle indirectly by potentiating the effects of various vasoconstrictor agents such as catecholaminesete. And these two mechanisms may play a role on the regulation of pulmonary and systemic arterial blood pressures.