Abstract
This study was designed to investigate the central action of circulating angiotensin II on the regulation of blood pressure in sodium depleted states. The effects of intravertebral arterial infusion of angiotensin II and [Sar-1, Ala-8] angiotensin II (saralasin) on plasma norepinephirne (NE) were studied in α-chloralose anesthetized dogs. Intravertebral arterial infusion of angiotensin II (10 ng/kg/min) increased mean arterial pressure (MAP), heart rate (HR) and plasma NE. Plasma NE was decreased by intravertebral arterial infusion of saralasin (0.40 ± 0.05 to 0.28 ± 0.04 ng/ml, p < 0.05) in normal dogs. The administration of furosemide produced significant increases in plasma NE ( 142.4 ± 23.7%, p < 0.01), plasma renin activity (PRA) (158.6 ± 26.3%, p < 0.01) and HR (32.3 ± 6.0 beats/min, p < 0.01). A slight rise in mean blood pressure (3.9 ± 1.2 mmHg, p < 0.05) was observed during the furosemide administration. Saralasin infused into the vertebral artery significantly suppressed the furosemide-induced increases in plasma NE, HR and PRA, and lowered mean arterial blood pressure. Intravenous infusion of the same dose of saralasin produced no changes in arterial blood pressure, HR and plasma NE. These results suggest that the central sympathetic potentiation induced by circulating angiotensin II may contribute to the regulation of blood pressure in sodium and volume depleted states produced by furosemide.
