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AJP - Heart and Circulatory Physiology, Vol 273, Issue 3 1075-H1081, Copyright © 1997 by American Physiological Society
ARTICLES |
C. Vandier, M. Delpech, M. Rebocho and P. Bonnet
Centre National de la Recherche Scientifique, Unite Mixte de Recherche 6542, Faculte des Sciences, Parc de Grandmont, Tours, France.
The effects of hypoxia on norepinephrine-induced contraction to explain why rabbit pulmonary arteries must be precontracted to observe a hypoxic response were studied. A force transducer was used to record the tone of isolated rabbit intrapulmonary artery rings placed in an organ chamber perfused with a physiological solution at 37 degrees C. Norepinephrine (10(-7) M) induced a phasic followed by a tonic contraction, and hypoxia increased the former and decreased the latter. Removal of external calcium (zero calcium solution) abolished the tonic contraction but left the phasic contraction intact. In the zero calcium solution, hypoxia increased the amplitude of the phasic contraction (9.8 +/- 7.4 vs. 13.3 +/- 11.9 mN) and decreased the 50% relaxation time (59 +/- 38 vs. 48 +/- 22 s). Hypoxia also increased the caffeine (5 mM)-induced contraction. This hypoxic increase in amplitude was abolished by ryanodine (100 microM). The hypoxic decrease in the 50% relaxation time was reduced by cyclopiazonic acid (1-10 microM). Therefore, hypoxia increases the reuptake of calcium by calcium pumps sensitive to cyclopiazonic acid in the caffeine- and ryanodine-sensitive stores.
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