Chronic hypoxia (CH) induces pulmonary artery hypertension (PAH), which in turn increases right cardiac afterload, right ventricular hypertrophia and eventually right cardiac failure. The aim on the study was to determine the impact of CH on basal PA resistance, independently from vasoreactivity in response to contractant and relaxant agonist.CH Wistar male rats (180-200 g) were maintained for 3 weeks in a hypobaric chamber (365 mmHg; 550 m simulated altitude) (n=5). Normoxic rats (N) were housed at normal atmospheric pressure (n=7). After euthanasia, the chest was opened, blood samples for hematocrit were obtained by left ventricular puncture, and the heart-lung block removed. The main PA was canulated, the left auricula was sectioned to allow perfusate efflux. The whole pulmonary vasculature was perfused through the canula at controlled pressure by a physiological saline solution, and the perfusion rate measured. Perfusion pressure (P, mmHg) and flow rate (FR, mL.s-1)) recordings were used to determine the pulmonary vascular resistance (R,mmHg.s.mL-1), considering R=P/FR. R values were plotted against P, and the P-R curve fitted by first-order exponential decay (R=Rmin+(Ro-Rmin)e-R.K, where Rmin is minimum resistance, Ro intercept of Y axis, and K (mmHg-1) the decay constant). Right cardiac hypertrophia was objectivised by Fulton index (right ventricular weight on left ventricular+septum weight). Statistical comparisons were done using Prism (Graphpad) software. Differences were considered significant when p<0.05. Hematocrite and Fulton index are from N versus CH rats were compared by Mann-Whitney test. Values are mean±SEM. Pressure-resistance curves from N versus CH rats were compared by first order exponential decay regression and F test. Best-fit parameters derived from non linear regression are given ±SD.In N rats, hematocrit and Fulton index were 51±1.6% and 0.26±0.018, respectively, and both significantly increased in CH rats (70±3.7% and 0.38±0.034). Basal pulmonary artery resistance, both in N and CH rats, exhibited an exponential decay shape against pressure. CH significantly increased overall basal vascular resistance (Fig. 1). In N rats, Ro=448.1±82.82, Rmin=-2.9±53.82, K=0.05±0.022, whereas in CH rats, Ro=982.6±230.80, Rmin=-63.3±45.98, K=0.084±0.026. These results show that basal pulmonary vascular resistance follows an exponential decay, which functional consequence is that increase in PA pressure is damped by decrease in pulmonary resistance. In CH rats, basal resistance is increased, which explains PAH at constant blood flow and subsequent right ventricular hypertrophy. This basal resistance increase, independent from vasoreactivity, may be due to pulmonary artery remodelling.