Mechanism of ouabain-induced contractions in guinea-pig tracheal rings
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1. The aim of the present study was to analyse the mechanism that underlies the force development induced by ouabain (ED100 = 100 μmol/L) in guinea-pig tracheal rings. 2. The dose-response curve showed that concentrations of ouabain above 100 μmol/L evoked smaller contractions. 3. Ouabain, at 100 μmol/L, produced two long-lasting consecutive transient contractions. The peak of the first contraction was 750 ± 75 mg, whereas the peak of the second contraction was 280 ± 46 mg. 4. Both contractions induced by ouabain were dependent on extracellular Ca2 . Consistent with this, verapamil (10 μmol/L) inhibited the first and second contractions by 77 and 59%25, respectively. 5. 3,4-Dichlorobenzamil (20 μmol/L) inhibited the first and second contractions by 68 and 97%25, respectively. 6. Simultaneous exposure to 15 mmol/L sodium solution and 100 μmol/L ouabain evoked only one transient contraction, larger (987 ± 135 mg) than either of the ouabain-induced contractions. 7. Inhibition of the sarcoendoplasmic reticulum Ca-ATPase with cyclopiazonic acid potentiated the first and second ouabain-induced contractions by 47 and 300%25, respectively. 8. Atropine (1 μmol/L) inhibited the first and second contractions by 44 and 76%25, respectively. 9. In conclusion, the results of the present study are relevant to the understanding of the mechanisms by which ouabain (100 μmol/L) contracts guinea-pig tracheal rings. At the muscular level, oubain induces Ca2 influx through L-type Ca 2 channels and the reverse mode of the sodium-calcium exchanger. At the nerve terminals, ouabain promotes the release of acetylcholine secondary to the increase in Ca2 influx mediated by the reverse mode of the sodium-calcium exchanger.
1. The aim of the present study was to analyse the mechanism that underlies the force development induced by ouabain (ED100 = 100 μmol/L) in guinea-pig tracheal rings. 2. The dose-response curve showed that concentrations of ouabain above 100 μmol/L evoked smaller contractions. 3. Ouabain, at 100 μmol/L, produced two long-lasting consecutive transient contractions. The peak of the first contraction was 750 ± 75 mg, whereas the peak of the second contraction was 280 ± 46 mg. 4. Both contractions induced by ouabain were dependent on extracellular Ca2%2b. Consistent with this, verapamil (10 μmol/L) inhibited the first and second contractions by 77 and 59%25, respectively. 5. 3,4-Dichlorobenzamil (20 μmol/L) inhibited the first and second contractions by 68 and 97%25, respectively. 6. Simultaneous exposure to 15 mmol/L sodium solution and 100 μmol/L ouabain evoked only one transient contraction, larger (987 ± 135 mg) than either of the ouabain-induced contractions. 7. Inhibition of the sarcoendoplasmic reticulum Ca-ATPase with cyclopiazonic acid potentiated the first and second ouabain-induced contractions by 47 and 300%25, respectively. 8. Atropine (1 μmol/L) inhibited the first and second contractions by 44 and 76%25, respectively. 9. In conclusion, the results of the present study are relevant to the understanding of the mechanisms by which ouabain (100 μmol/L) contracts guinea-pig tracheal rings. At the muscular level, oubain induces Ca2%2b influx through L-type Ca 2%2b channels and the reverse mode of the sodium-calcium exchanger. At the nerve terminals, ouabain promotes the release of acetylcholine secondary to the increase in Ca2%2b influx mediated by the reverse mode of the sodium-calcium exchanger.
