TY - JOUR
T1 - Effects of hypoxia upon contractions evoked in isolated rabbit pulmonary artery by potassium and noradrenaline.
AU - Marriott, J. F.
AU - Marshall, J. M.
PY - 1990/3/1
Y1 - 1990/3/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0025319719&partnerID=8YFLogxK
U2 - 10.1113/jphysiol.1990.sp017969
DO - 10.1113/jphysiol.1990.sp017969
M3 - Article
C2 - 2352177
AN - SCOPUS:0025319719
SN - 0022-3751
VL - 422
SP - 15
EP - 28
JO - The Journal of Physiology
JF - The Journal of Physiology
IS - 1
ER -