Renin-angiotensin system on systemaic, pulmonary and renal circulation in actue respiratory acidosis with special reference to the role of angiotensin II

The elevation of plasma renin activity (PRA) during actue respiratory acidosis in dogs was reported. In present study, the influence of renin-angiotensin (R-A) system especially, angiotensin II (AT II) on systemic, pulmonary and renal circulations in actue respiraty acidosis was evaluated. Fifteen mongrel dogs were anesthetized with sodium pentobalbital and inhalated with 15% carbon dioxide (CO_2) in room air (Exam.1). 7 of them during CO_2 inhalation were administered exogenous AT II 30ng/kg min iv. (Exam.2). [sar^1-ile-8] AT II were given to another 8 of them (Exam.3). Mean aortic presuure (mAoP), total systemic vacular resitance (TSVR), pulmonary artery pressure (PAP), total plumonary resistance (TPR), renal blood flow (RBF), renal vascular resistance (RVR) and cardiac output (CO) were measured. PRA and AT II were measured by radiommunoassey. In severe respiratory acidosis, pH being 7.006±0.044 and PaCO_2 103.5±9.6mmHg, PRA elevated from 9.7±5.7ng/ml/hr to 33.2±13.8nh/ml/hr and AT II also elevated from 74.4±55.1pg/ml to 345.2±231.6pg/ml. mAoPand TSVR decreased, while PAP and TOR increased. RBF decreased, while RVR had to change. In exam. 2, mAoP and TSVR increased. PAP also increased, while TPR had not significant change. RBF decreased, while RVR increased. In exam. 3, mAoP and TSVR decreased. RBF was increased and RVR decreased. Whereas, PAP and TPR were not changed. Namely, AT II played a roll of pressure elevating factor on systemic circulation, and decreasing factor to RBF. On the other hand, in pulmonary circulation AT II played a less important roll in elevated PAP. These results suggest that the response to AT II on systemic, pulmonary and renal, circulations in severe respiratory acidosis was different each other.