Abstract
1. Comparisons have been made between rabbit thoracic aorta and main pulmonary artery of the effects of hypoxia upon contractions evoked by noradrenaline (NA) and KCl (K+). 2. Contractions were evoked in cylindrical sections of pulmonary artery and aorta, mounted for isometric recording of tension, by NA and K+ (at ED80) in normoxia (PO2 110 mmHg) and hypoxia (PO2 23 or 7 mmHg). Contractions were also evoked in Ca2(+)-free conditions with EGTA to prevent influx of extracellular Ca2+. All contractions are expressed as a percentage of normoxic response in the presence of Ca2+. 3. Potassium-evoked contractions of aorta and pulmonary artery were reduced to a similar extent by both levels of hypoxia, to 85 and 92% respectively. As expected K(+)-evoked contractions were virtually abolished by Ca2(+)-free conditions. It is proposed that hypoxia has a small inhibitory effect upon contraction mediated by Ca2+ influx via voltage-operated Ca2+ channels. 4. In the aorta in the presence of Ca2+, hypoxia reduced NA-evoked contractions to 84% at PO2 23 mmHg and 34% at PO2 7 mmHg. In the absence of Ca2+, NA-evoked contractions reached 73% in normoxia, but only 43 and 21% at PO2 23 and 7 mmHg respectively. These results suggest that hypoxia reduces the component of contraction that is mediated by release of intracellular Ca2+ and possibly that mediated by agonist-induced Ca2+ influx. 5. In the pulmonary artery also, NA-evoked responses in the absence of Ca2+ were reduced from 60% in normoxia, to 49 and 38% at PO2 23 and 7 mmHg. But, in the presence of Ca2+, hypoxia potentiated NA-evoked contractions to 113 and 111% at PO2 23 and 7 mmHg respectively. It is proposed that in the pulmonary artery, hypoxia reduces the component of contraction mediated by release of intracellular Ca2+, but facilitates that mediated by extracellular Ca2+. Possible mechanisms are discussed.