During acute hypercapnia vasopressin inhibits an angiotensin drive to ventilation in conscious dogs.
J Appl Physiol (1985)
; 79(3): 786-94, 1995 Sep.
Article
in En
| MEDLINE
| ID: mdl-8567518
ABSTRACT
Intravenous infusion of arginine vasopressin (AVP) depresses the slope of the ventilatory response to CO2 during acute hypercapnia. We therefore tested the hypothesis that AVP V1-receptor blockade would increase the slope of the ventilatory response to CO2. After a 20-min control period, an AVP V1-receptor antagonist (d(CH2)5[Tyr(Me)2]AVP) was injected into six conscious resting dogs. Thirty minutes after AVP V1-receptor blockade, dogs were exposed to sequential 20-min periods of 5 and 6.5% inspired CO2 in air. A second protocol (no AVP V1-receptor blockade) was conducted as a control. As predicted, AVP V1-receptor blockade enhanced ventilation during inhalation of 6.5% CO2 in association with an increased metabolic rate and increased plasma angiotensin II (ANG II). In eupneic dogs, stimulation of respiration by AVP V1-receptor blockade is mediated by ANG II. A third protocol with ANG II-receptor blockade (intravenous infusion of saralasin) combined with AVP V1-receptor blockade indicated that ANG II mediated the increase in metabolism and the augmented ventilation during inhalation of 6.5% CO2. We conclude that during acute hypercapnia of sufficient magnitude, and perhaps duration, AVP inhibits an ANG II-mediated stimulation of metabolism and respiration.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Respiration
/
Angiotensin II
/
Arginine Vasopressin
/
Antidiuretic Hormone Receptor Antagonists
/
Hemodynamics
/
Hypercapnia
Limits:
Animals
Language:
En
Journal:
J Appl Physiol (1985)
Journal subject:
FISIOLOGIA
Year:
1995
Type:
Article
Affiliation country:
Canada