Acute hypoxic pulmonary vasoconstriction in conscious dogs decreases renin and is unaffected by losartan

Abstract

Acute hypoxic pulmonary vasoconstriction (HPV) may be mediated by vasoactive peptides. We studied eight conscious, chronically tracheostomized dogs kept on a standardized dietary sodium intake. Normoxia (40 min) was followed by hypoxia (40 min, breathing 10% oxygen, arterial oxygen pressures 36 ± 1 Torr) during both control (Con) and losartan experiments (Los; iv infusion of 100 μg ⋅ min−1 ⋅ kg−1losartan). During hypoxia, minute ventilation (by 0.9 l/min in Con, by 1.3 l/min in Los), cardiac output (by 0.36 l/min in Con, by 0.30 l/min in Los), heart rate (by 11 beats/min in Con, by 30 beats/min in Los), pulmonary artery pressure (by 9 mmHg in both protocols), and pulmonary vascular resistance (by 280 and 254 dyn ⋅ s ⋅ cm−5in Con and Los, respectively) increased. Mean arterial pressure and systemic vascular resistance did not change. In Con, PRA decreased from 4.2 ± 0.7 to 2.5 ± 0.5 ng ANG I ⋅ ml−1 ⋅ h−1, and plasma ANG II decreased from 11.9 ± 3.0 to 8.2 ± 2.1 pg/ml. The renin-angiotensin system is inhibited during acute hypoxia despite sympathetic activation. Under these conditions, ANG II AT1-receptor antagonism does not attenuate HPV.