Chronic ventilatory hypoxia results in remodelling of pulmonary vasculature and hypoxic pulmonary hypertension. Hypoxia increases the turnover of extracellular matrix proteins in peripheral pulmonary blood vessels. We studied hypoxia – induced changes in collagen isolated from pulmonary peripheral arteries and from systemic mesenteric peripheral arteries. Our hypothesis is that presence of collagen cleavage products in the walls of hypoxic peripheral pulmonary arteries starts the vascular remodelling. Two groups of rats were exposed to hypoxia (FiO2 = 0,1) for four days (pulmonary arteries – H4, N=7 – and mesenteric arteries – systH4, N=6) and three weeks (pulmonary arteries – H21, N=7 and mesenteric arteries – systH21, N=6). Two relevant control groups were kept in air. Collagen proteins ex¬tracted from arteries by limited pepsin digestion were studied using SDS polyacryl amide electrophoresis and Western blot. Presence of collagenolytic enzyme, matrix metalloproteinase-13 (MMP-13) and inducible NO synthase (iNOS) were also studied using Western blot. In the peripheral pulmonary arteries of rats exposed to hypoxia three weeks we found already described ~75 kDa cleavage fragment (three-fourth fragment of collagen type I molecule) but not its one-fourth (~25 kDa) counterpart. In peripheral pulmonary arteries of rats exposed to 4 days hypoxia, however, both three-fourth and one-fourth fragments of collagen type I and type III were identified. In the control normoxic group no collagen cleavages were detected in lung vessels. Three-fourth and one fourth fragments of collagen type I were found also in mesenteric peripheral arteries of rats exposed four days to hypoxia but theirs relative density was significantly lower than in lung vessels. MMP-13 and iNOS were detected in early phase of pulmonary hypoxic hypertension in peripheral pulmonary arteries but not in arteries of rats exposed to hypoxia three weeks or any systemic vessels. We interpret breakdown of collagen to one-fourth and three-four fragments in an early phase of hypoxia exposure as a result of relative low resistance of poorly cross-linked molecule to proteolysis by specific MMPs. Resulting accumulation of collagen cleavages (“matrikines”) stimulates the fibrotization of prealveolar pulmonary vessels.