Respiratory stimulation by angiotensin II

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.