Arginine vasopressin and baroreflex function after converting
enzyme inhibition in normal humans.
Goldsmith, Steven R.
Hennepin County Medical Center and the University of Minnesota,
Minneapolis, Minnesota
APStracts 4:0005E, 1997.
Background: 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 is inhibited. Objective: To test
the hypothesis that a modest physiologic 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 following pretreatment with
lisinopril in healthy human volunteers. Methods: 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) were infused for 15 minutes double-blind on the first two
days. Baroreflexes were then perturbed as follows: 15 minutes 60
head-up tilt, 15 minutes 30 head-down tilt plus 1000 cc normal saline
infusion, 15 minutes 30 head-down tilt plus phenylephrine titrated to
raise mean arterial pressure 10-15 mm Hg. The study was repeated on a
third day 12 hours after 5 mg of lisinopril. Five additional subjects
underwent similar baroreflex study on two days with only lisinopril
and placebo. Results Prior to 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 <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. Conclusion: 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 responses. 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.
Received 16 April 1996; accepted in final form 25 July 1996.
APS Manuscript Number E187-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 21 January 1997