Contractility of the myocardium is determined by the interaction of contractile (actin and myosin) and regulatory (troponin and tropomyosin) proteins in the presence of calcium ions and chemical energy. The formation of the actomyosin complex is affected by the modulatory (C-, F-, M-proteins, actinins) and interstitial proteins (different types of collagens, glycoproteins, glycosaminoglycans, elastins). Cardiac hypoxia is accompanied by qualitative and quantitative changes in both collagenous (change in the proportion of different extracellular matrix proteins) and non-collagenous proteins (formation of different isomyosins and isoforms of actins or regulatory proteins). This remodelling of cardiac musculature influences significantly the process of contraction and relaxation in the hypoxic myocardium.
The effect of chronic administration of angiotensin converting enzyme inhibitor on the development of hypoxic pulmonary hypertension was studied in rats. Male Wistar rats were exposed for 3 weeks to isobaric hypoxia (10 % O2) and treated with 10 mg/kg b.w. of Ramipril daily. The haemodynamic properties of the pulmonary vasculature were then measured in isolated blood-perfused lung preparation. Ramipril administration during the sojourn in hypoxia resulted in lower baseline perfusion pressure and lower slope of perfusion pressure-flow relationship compared to non-treated hypoxic rats. Partitioning of the distribution of pulmonary vascular resistance across the vascular bed by the occlusion technique showed that it was mainly due to a decrease of arterial and venous vascular resistances to blood flow. It is suggested that Ramipril attenuates the process of morphological reconstruction of pulmonary vasculature by chronic hypoxia rather than the level of vascular smooth muscle tone.