Effect of calcium and calmodulin antagonists on contractile responses of the human uterine artery.
1. The dependence on extracellular calcium of contractile responses of intramyometrial arteries (0.5-2 mm diameter), as well as the effects of various types of calcium antagonists on these responses, were studied. Contractions were induced by K-depolarization (K) and noradrenaline (NA). 2. Whereas the K response was completely abolished in a calcium-free medium containing 2 mM LaCl3, the NA response was substantially maintained. 3. Nimodipine strongly inhibited the K response but had a relatively weak effect on the NA response; the IC50 values for the K and NA responses being 2 nM and 6 microM, respectively. Corresponding values for verapamil were about 0.7 and 10 microM. 4. Calmodulin antagonists, particularly trifluoperazine and flunarizine, caused a greater inhibition of the NA than of the K response. 5. These results indicate that besides the extracellular calcium which appears to be the major source of activator calcium, there is an intracellular pool of calcium which can be utilized to activate, albeit to a limited extent, drug-induced contractile responses.
Kostrzewska
A
A
Institute of Obstetrics and Gynaecology, Medical School, Bialystok, Poland.
Laudanski
T
T
Batra
S
S
D002118:Calcium / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002147:Calmodulin / Q000037:antagonists & inhibitors*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011247:Pregnancy
D002121:Calcium Channel Blockers; D002147:Calmodulin; D011189:Potassium Chloride; D002118:Calcium; D009638:Norepinephrine