Intravenous angiotensin infusion increased mean aortic blood pressure by 58 +/- 12 mmHg, with about half of this rise due to increased end-diastolic volume caused by blood redistribution.
Does intravenous angiotensin infusion increase blood pressure via increased preload from blood redistribution in anesthetized dogs?
About half of the blood pressure elevation during angiotensin infusion is driven by increased preload due to blood redistribution, primarily from the splanchnic bed.
The mechanism of increased preload and its contribution to the rise in blood pressure during intravenous angiotensin infusion were studied in anesthetized dogs. In open-chest dogs angiotensin increased mean aortic blood pressure by 58 +/- 12 mmHg. Left ventricular end-diastolic dimension, measured as myocardial chord length (MCL) by ultrasonic technique, increased by 7 +/- 1%. By inflating a balloon in the inferior vena cava, end-diastolic MCL was reduced to control value and the rise in mean aortic blood pressure was almost halved to 32 +/- 10 mmHg above control value. A similar preload effect was recorded in closed-chest dogs using end-diastolic left ventricular pressure as an estimate of left ventricular volume. During angiotensin infusion to the upper body only, end-diastolic MCL did not increase. When redistribution of the splanchnic blood volume was prevented, the effect of angiotensin on end-diastolic MCL was reduced to 1/3. Angiotensin reduced liver but not splenic dimension measured by ultrasonic technique. We conclude that about half of the rise in blood pressure during angiotensin infusion is due to increased end-diastolic volume caused by blood redistribution. About 2/3 of this increase in preload is due to redistribution from the splanchnic bed, mainly from the liver.
Stokland et al. (1982) studied this question. Intravenous angiotensin infusion vs. Baseline control was evaluated on Mean aortic blood pressure and left ventricular end-diastolic dimension. Intravenous angiotensin infusion increased mean aortic blood pressure by 58 +/- 12 mmHg, with about half of this rise due to increased end-diastolic volume caused by blood redistribution.