Physiological increases in arginine vasopressin (AVP) have been shown to potentiate baroreflex activity in experimental animals. Pharmacological amounts of AVP have been shown to decrease sympathetic nervous system activity in humans, whereas the role of smaller increases in plasma AVP is unclear, either for baroreflex function or sympathetic activity. The present study tested the hypotheses that in normal humans physiological increases in plasma AVP would 1) decrease basal sympathetic nervous system activity as measured by systemic venous norepinephrine (NE) spillover; 2) enhance or restrain the increases in heart rate (HR), forearm vascular resistance, and NE spillover during baroreceptor unloading during head-up tilt; and 3) augment the decline in HR and NE spillover during baroreceptor loading with head-down tilt and/or with phenylephrine infusion plus head-down tilt. In the baroreceptor unloading studies, HR, arterial pressure, forearm blood flow, plasma NE, NE clearance, and NE spillover were assessed during infusions of AVP (plasma AVP 16-20 pg/ml) or vehicle (given double blind) in the supine position. All variables then were assessed during 15 min of head-up tilt. In the baroreflex loading studies, the same assessments (except forearm blood flow) were made during 15 min of head-down tilt followed by 15 min of head- down tilt plus phenylephrine. Compared with vehicle, AVP had no effect on the responses of any variable in the supine position or on the expected reflex responses during head-up tilt and head-down tilt plus phenylephrine. These data argue against an important role for AVP at increased but still physiological levels in the regulation of either baseline sympathetic nervous system activity or the responses to mild perturbations of baroreflex activity in normal humans.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||6 35-6|
|State||Published - 1994|
- norepinephrine spillover
- sympathetic nervous system