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

Acute hypoxic pulmonary vasoconstriction (HPV) may be mediated by vasoactiv e peptides. We studied eight conscious, chronically tracheostomized dogs ke pt 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 infusio n of 100 mu g.min(-1).kg(-1) losartan). 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 i n Con, by 0.30 l/min in Los), heart rate (by 11 beats/min in Con, by 30 bea ts/min in Los), pulmonary artery pressure (by 9 mmHg in both protocols), an d pulmonary vascular resistance (by 280 and 254 dyn.s.cm(-5) in Con and Los , respectively) increased. Mean arterial pressure and systemic vascular res istance 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 h ypoxia despite sympathetic activation. Under these conditions, ANG II AT(1) -receptor antagonism does not attenuate HPV.