The calcium dependence of histamine, carbachol and potassium chloride-induced contraction in human airways in vitro.
The effect of depletion of calcium from the Krebs Henseleit (KH) solution and the addition of EDTA (1 mM) on contraction of human isolated bronchus by histamine, carbachol and potassium chloride (KCl) was examined. Contractions to histamine and carbachol were almost totally abolished in calcium free KH in the presence of 1 mM EDTA which only reduced KCl responses to 76% of control values. Verapamil (10(-6), 10(-5), 10(-4) M) decreased histamine and KCl contractile responses in a dose-related manner while having no significant effect on carbachol-induced tension. The intracellular calcium antagonist TMB8 10(-4) M caused a slight but significant decrease in histamine contraction but was without effect on the maximal response of the other two agonists. TMB8 decreased the potency of both histamine and carbachol. These results suggest that histamine, carbachol and KCl utilise different pools of calcium for contraction, that only part of the calcium entry for all agonists occurs via voltage-dependent calcium channels and that intracellular calcium stores may play a small role in contraction to these agonists.
D001980:Bronchi / Q000187:drug effects* / Q000502:physiology; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D005707:Gallic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects*; D011189:Potassium Chloride / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; C006014:8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; D005707:Gallic Acid; D011189:Potassium Chloride; D006632:Histamine; D002217:Carbachol; D014700:Verapamil; D002118:Calcium