Key result
Calcium entry blockers and calmodulin inhibitors inhibited 5-HT-, K+-, and CaCl2-induced contractions in human isolated umbilical artery, with mechanisms differing from other vascular beds.
Why the study?
Do calcium entry blockers and calmodulin inhibitors reduce 5-HT-, K+-, and Ca2+-induced contractions in human isolated umbilical artery?
Do calcium entry blockers and calmodulin inhibitors reduce 5-HT-, K+-, and Ca2+-induced contractions in human isolated umbilical artery?
Calcium entry blockers and calmodulin inhibitors exhibit distinct inhibitory profiles on contractions in human umbilical arteries compared to other vascular beds.
Should not alter clinical management of umbilical artery tone; leaves open whether calcium inhibition differs meaningfully in vivo from other vascular beds.
The effects of calcium (Ca2+) withdrawal, Ca2+ entry blockers and calmodulin inhibitors on the contractile responses to 5-hydroxytryptamine (5-HT), K+ and CaCl2 have been studied in human isolated umbilical artery. Following Ca2+ withdrawal from the medium (30 min), both 5-HT- and K(+)-induced contractions were virtually abolished. Ca2+ entry blockers (nifedipine, verapamil, diltiazem and cinnarizine) were significantly more effective in inhibiting 5-HT- than K(+)-induced contractions. In relation to calmodulin inhibitors, trifluoperazine inhibited all types of contractions, whereas W-7 (N-6-aminohexyl-5-chloro-1-naphthalene sulphonamide) only inhibited 5-HT- and CaCl2-induced contractions. All drugs inhibited CaCl2-induced contractions in a non-competitive manner. These findings indicate that the mechanisms by which these drugs exert their inhibitory effects on human umbilical artery are markedly different from those reported in other vascular beds.
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Medeiros et al. (1991) studied this question. Calcium entry blockers and calmodulin inhibitors was evaluated on Contractile responses to 5-HT, K+, and CaCl2. Calcium entry blockers and calmodulin inhibitors inhibited 5-HT-, K+-, and CaCl2-induced contractions in human isolated umbilical artery, with mechanisms differing from other vascular beds.
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