Effect of BQ123 on vasoconstriction as a result of either hypoxia or endothelin‐1 in perfused rat lungs

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Abstract
A possible role of endothelin (ET)‐1 in mediating hypoxic pulmonary vasoconstriction (HPV) was examined by comparing haemodynamic differences between ET‐1‐induced vasoconstriction and HPV in isolated perfused rat lungs. An ETA receptor antagonist (BQ123) was also employed to assess the effects of ET‐1. The pulmonary arterial pressure (Ppa) was significantly increased by alveolar hypoxia (3% O2) and by ET‐1 (5 nM). The pulmonary microvascular pressure was not changed by hypoxia, but increased more than two‐fold by ET‐1 (P < 0.01). Hypoxia significantly increased pulmonary arterial resistance (P < 0.01) while ET‐1 significantly increased pulmonary venous resistance (P < 0.01), and slightly increased arterial resistance. Lung weight was increased by ET‐1 and decreased by hypoxia, accompanied by similar Ppa responses in both cases. BQ123 (10‐6 m and 10‐5 m) did not influence the changes in Ppa and lung weight induced by hypoxia or angiotensin II (0.3 μg). BQ123 did, however, suppress (P < 0.05) the increase in Ppa and lung weight induced by 5 nM ET‐1. Thus, it appears unlikely that ET‐1 is involved in changes in pulmonary vascular tone during acute HPV.

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