To determine whether removal of inhibition of arginine vasopressin (AVP) by vagal afferents results in persistent elevation of plasma AVP, effects of bilateral cervical vagal denervation (VD) on plasma AVP were examined in 10 dogs with sinoaortic baroreceptor denervation (SAD). VD increased plasma AVP levels by 98 ± 16 from 3.8 ± 1.0 pg/ml (P<0.01) at 15 min after VD. By 4 h after VD there were no significant differences from control values. Responses of plasma AVP were also examined in response to acute volume expansion in conscious dogs with all reflexes intact, SAD, and SAD plus VD. In intact and SAD dogs, when blood volume was expanded by 20% with a rapid infusion of isotonic, isooncotic 3% dextran in saline, mean left atrial pressure rose transiently and plasma AVP fell insignificantly. With more prolonged stimulation to cardiopulmonary receptors, i.e., when left atrial pressure was maintained at elevated levels for 1 h by volume loading, plasma AVP fell by 0.9 ± 0.3 pg/ml. However, after correction for hemodilution was made, AVP did not change with volume expansion, indicating that secretion rate was unchanged. Thus acute, but not chronic, interruption of vagal pathways induces striking release of AVP, but a resetting mechanism rapidly returns plasma AVP to control levels. Furthermore, stimulation of vagally innervated receptors by means of acute volume expansion suppresses plasma AVP when the elevation in atrial pressure is sustained, but this fall in plasma AVP can be accounted for entirely by the concomitant hemodilution.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||1 (20/1)|
|State||Published - 1986|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)