Arginine vasopressin and baroreflex function after converting enzyme inhibition in normal humans

Arginine vasopressin (AVP) has been shown to interact with sinoaortic and cardiac reflexes under selected experimental conditions. In humans, there is no evidence that AVP potentiates reflex function at modestly increased plasma levels, except possibly if the angiotensin-converting enzyme (ACE) is inhibited. The objective of this study was to test the hypothesis that a modest physiological increase in plasma AVP would potentiate the responses of heart rate (HR), forearm vascular resistance (FVR), plasma norepinephrine (NE), or systemic NE spillover to baroreflex unloading and loading after pretreatment with lisinopril in healthy human volunteers. Seven normal young men were studied on three occasions. Baseline HR, FVR, and steady-state NE kinetics were established, and AVP or vehicle (5% dextrose in water) was infused for 15 min double-blind on the first 2 days. Baroreflexes were then perturbed as follows: 15 min 60°head-up tilt, 15 min 30°head-down tilt plus 1,000 ml normal saline infusion, 15 min 30°head-down tilt plus phenylephrine titrated to raise mean arterial pressure 10-15 mmHg. The study was repeated on a third day 12 h after 5 mg of lisinopril. Five additional subjects underwent similar baroreflex study on 2 days with only lisinopril and placebo. Before baroreflex deactivation and activation in the absence of lisinopril, AVP infusion had no hemodynamic or neurohormonal effects. During AVP infusion after lisinopril, HR decreased from 67 ± 6.5 to 62 ± 4.5 beats/min (P < 0.05). AVP had no effect on the response of any variable during baroreflex perturbation relative to vehicle, either with or without lisinopril. Lisinopril had no independent effect on these responses in the additional five subjects. At modestly increased plasma levels, AVP did not affect the responses of HR, FVR, plasma NE, or systemic NE spillover to baroreflex deactivation and activation. After lisinopril, AVP infusion produced a modest bradycardia but still had no significant positive effect on either response. These data suggest that inhibition of the angiotensin- converting enzyme may unmask mild direct or vagally mediated effects of AVP on HR but does not unmask baroreflex potentiation.