Premium
Early and late contraction induced by ouabain in human umbilical arteries
Author(s) -
Sato Koichi,
Aoki K.
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb09821.x
Subject(s) - ouabain , verapamil , contraction (grammar) , caffeine , chemistry , diltiazem , muscle contraction , medicine , sodium , monensin , calcium , endocrinology , nifedipine , biochemistry , organic chemistry
1 Ouabain (3 × 10 −7 –10 −4 m ) evoked a biphasic contraction in human umbilical artery that consisted of an early and a late contraction. The Ca 2+ ‐antagonists, verapamil (10 −7 –10 −5 m ), diltiazem (10 −7 –10 −5 m ) and nifedipine (10 −9 –10 −7 m ) inhibited the early but not the late contraction. Caffeine (5 m m ) changed neither the magnitude of the peak of the biphasic contraction nor the time needed to reach it. 2 Sodium concentration reduction (140 to 0 m m , replaced by N‐methyl‐ d ‐glucamine, NMG) produced dose‐dependent contraction of the arterial strip in 2.5 m m Ca 2+ solution after the first treatment with verapamil (10 −5 m ) and caffeine (5 m m ), but not in Ca 2+ ‐free solution. 3 After prior treatment with verapamil and caffeine, the amplitude of the ouabain (10 −4 m )‐induced late contraction varied, depending on the concentration of Ca 2+ (0–2.5 m m ) in the medium. 4 Amiloride (5 × 10 −5 m –5 × 10 −4 m ), an inhibitor of the Na + –Ca 2+ exchange system, produced dose‐dependent inhibition of the late contraction induced by ouabain (10 −5 m ) after prior treatment with verapamil and caffeine. 5 The time needed to reach the peak tension induced by monensin (5 × 10 −7 m ) together with ouabain (10 −6 m ) was less than that with ouabain alone, but the magnitude of the peak tension was not changed. 6 These results suggest that the early and late contractions caused by ouabain respectively produce a Ca 2+ influx through voltage‐sensitive Ca 2+ channels and Ca 2+ entry through sodium‐calcium (Na + — Ca 2+ ) exchange.