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J Appl Physiol 87: 2284-2289, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 6, 2284-2289, December 1999

ET-1-induced pulmonary vasoconstriction shifts from ETA- to ETB-receptor-mediated reaction after preconstriction

Joachim Schmeck, Heidi Gluth, Nicolas Mihaljevic, Michael Born, Martina Wendel-Wellner, and Peter Krafft

Department of Anesthesiology and Operative Intensive Care Medicine, University Hospital Mannheim, University of Heidelberg, 68135 Mannheim, Germany

Endothelin-1 (ET-1) has been reported to induce pulmonary vasoconstriction via either ETA or ETB receptors, and vasorelaxation after ET-1 injection has been observed. Our study investigated the effects of ET-1 in isolated rabbit lungs, which were studied at basal tone (part I) and after preconstriction (U-46619; part II). Pulmonary arterial pressure (PAP) and lung weight gain were monitored continuously. In part I, ET-1 (10-8 M; n = 6; control) was injected after pretreatment with the ETA-receptor antagonist BQ-123 (10-6 M; n = 6) or the ETB-receptor antagonist BQ-788 (10-6 M; n = 6). The same protocol was carried out in part II after elevation of pulmonary vascular tone. ET-1 induced an immediate PAP increase (Delta PAP 4.3 ± 0.4 mmHg at 10 min) that was attenuated by pretreatment with BQ-123 (P < 0.05 at 10 min and P < 0.01 thereafter) and that was more pronounced after BQ-788 (P < 0.01 at 10 min and P < 0.001 thereafter). In part II, ET-1 induced an immediate rise in PAP with a maximum after 5 min (Delta PAP 6.3 ± 1.4 mmHg), leveling off at Delta PAP 3.2 ± 0.2 mmHg after 15 min. Pretreatment with BQ-123 failed to attenuate the increase. BQ-788 significantly reduced the peak pressure at 5 min (0.75 ± 0.4 mmHg; P < 0.001) as well as the plateau pressure thereafter (P < 0.01). We conclude that ET-1 administration causes pulmonary vasoconstriction independent of basal vascular tone, and, at normal vascular tone, the vasoconstriction seems to be mediated via ETA receptors. BQ-788 treatment resulted in even more pronounced vasoconstriction. After pulmonary preconstriction, ETA antagonism exerted no effects on PAP, whereas ETB antagonism blocked the PAP increase. Therefore, ET-1-induced pulmonary vasoconstriction is shifted from an ETA-related to an ETB-mediated mechanism after pulmonary vascular preconstriction.

BQ-123; BQ-788; endothelin; preconstriction


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