Sj. Heitman et Db. Jennings, ANGIOTENSIN-II MODULATES RESPIRATORY AND ACID-BASE RESPONSES TO PROLONGED HYPOXIA IN CONSCIOUS DOGS, American journal of physiology. Regulatory, integrative and comparative physiology, 44(2), 1998, pp. 390-399
We tested the hypothesis that angiotensin II(ANG II) contributes to ve
ntilatory and acid-base adaptations during 3-4 h of hypoxia (partial p
ressure of O-2 in arterial blood approximate to 43 Torr) in the consci
ous dog. Three protocols were carried out over 3-4 h in five dogs: 1)
air control, 2) 12% O-2 breathing, and 3) 12% O-2 breathing with ANG I
I receptors blocked by infusion of saralasin (0.5 mu g kg(-1).min(-1))
. After 2 h of hypoxia, expired ventilation and alveolar ventilation p
rogressively increased, and the partial pressure of CO2 in arterial bl
ood and the difference between the arterial concentrations of strong c
ations and strong anions ([SID]) decreased. When the hypoxic chemorece
ptor drive to breathe was abolished transiently for 30 s with 100% O-2
, the resultant central apneic time decreased between 0.5 and 2.5 h of
hypoxia. All these adaptive responses to hypoxia were abolished by AN
G II receptor block. Because plasma ANG II levels were lower during hy
poxia and hypoxic release of arginine vasopressin from the pituitary i
nto the plasma was prevented by ANG II receptor block, the brain renin
-angiotensin system was likely involved. It is possible that ANG II me
diates ventilatory and acid-base adaptive responses to prolonged hypox
ia via alterations in ion transport to decrease [SID] in brain extrace
llular fluid rather than acting by a direct neural mechanism.