Experimental angiotensin II hypertension.

The mechanisms by which angiotensin II (AII) produces hypertension was studied in a group of 13 large dogs maintained on a Na intake of 200 meq/day. AII was infused at 10 ng x kg-1 x min-1 iv for 8 days. Arterial pressure increased from the control level of 98 +/- 3 to 160 +/- 7 mmHg and cardiac output fell significantly from the control value of 3.4 +/- 0.2 to 2.4 +/- 0.2 and 2.6 +/- 0.1 l/min on the 5th and 8th days of AII infusion. Mean circulatory filling pressure (MCFP) rose from the control mean of 9.5 +/- 0.5 to 11.6 +/- 0.9 (P < 0.05) and 12.6 +/- 0.6 mmHg (P ¿ 0.05) on the 5th and 8th day of infusion. On the 1st day of AII infusion, approximately 70 meq Na was retained; this retention persisted until the 4th day, when a marked natriuresis returned the dogs to Na balance. 22Na space increased slightly (P < 0.05) during the early part of the study, but fell back to the control level by the 5th day of infusion. Blood volume was unchanged throughout the study. The marked increase observed in MCFP with unchanged blood volume indicates that the unstressed volume or compliance of the circulatory system must have decreased. In this form of hypertension, the increase in arterial pressure was achieved without volume expansion and cardiac output elevation, but with large initial increases in arterial and venous vascular tone.