Effects of extracellular calcium and of the calcium entry blockers flunarizine and nimodipine on contractile responses in human temporal arteries.
Contraction induced by 124 mM potassium followed the depolarization of smooth-muscle cells and activation of potential-operated calcium channels in human temporal arteries. The contraction elicited consisted of two phases, one rapid and one slowly developing stable phase; both were affected by the two calcium entry blockers flunarizine and nimodipine but at significantly different concentrations. In calcium-free medium 124 mM potassium resulted in a weak contraction. Addition of calcium caused a concentration-dependent contraction that was attenuated by the calcium entry blockers at concentrations comparable to those inhibiting the second phase. The results suggested that in human temporal arteries flunarizine and nimodipine act as calcium entry blockers; there was good correlation with the therapeutic plasma concentration for nimodipine but not for flunarizine.
D002118:Calcium / Q000494:pharmacology; D005444:Flunarizine / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008881:Migraine Disorders / Q000503:physiopathology / Q000517:prevention & control*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009553:Nimodipine / Q000494:pharmacology* / Q000627:therapeutic use; D011188:Potassium / Q000494:pharmacology; D013699:Temporal Arteries / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects*
D009553:Nimodipine; D005444:Flunarizine; D011188:Potassium; D002118:Calcium