Chronic Angiotensin II Infusion Decreases Renal Norepinephrine Overflow in Conscious Dogs

Sympathetic nerve activity and in particular renal sympathetic nerve activity were monitored in six conscious dogs subjected to 6 days of intravenous angiotensin (ANG II) infusion (20 ng/kg/min). This was accomplished by measurement of both arterial and renal venous plasma catecholamine concentration. During the initial 4 hours of ANG II infusion, mean arterial pressure (MAP) increased 35 ± 8 mm Hg from a control value of 101 ± 4 mm Hg. Although there were no significant changes in arterial plasma norepinephrine (NE) concentration at this time (control = 148 ± 40 pg/ml), arterial plasma epinephrine (E) concentration increased threefold (control 42 ± 15 pg/ml). After 24 hours of ANG II infusion, MAP remained elevated (132 ± 5 mm Hg), but plasma E concentration returned to control levels. From Days 2 through 6 of ANG II infusion, MAP was elevated approximately 40 mm Hg, but there were no chronic increases in either arterial plasma E or NE concentrations. In contrast to arterial plasma catecholamine concentration, renal vein plasma NE concentration (control = 216 ± 27 pg/ml) actually decreased during both the acute (122 ± 12 pg/ml) and chronic (103 ± 26 pg/ml) phases of ANG II infusion. Moreover, renal NE overflow (renal venous plasma NE concentration- arterial plasma NE concentration × effective renal plasma flow), an index of renal sympathetic nerve activity, was depressed during the chronic phase of ANG II hypertension. These results, therefore, do not support the contention that the sympathetic nervous system mediates the hypertension produced by elevated plasma levels of ANG II. In fact, the finding that renal NE overflow is chronically depressed during long-term ANG II infusion suggests that changes in renal sympathetic activity may serve to attenuate the development of elevated arterial pressure during ANG II hypertension.