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Monovalent cation and L‐type Ca 2+ channels participate in calcium paradox‐like phenomenon in rabbit aortic smooth muscle cells
Author(s) -
Zakharov Sergey I.,
Mongayt Dmitry A.,
Cohen Richard A.,
Bolotina Victoria M.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.071af.x
Subject(s) - extracellular , egta , nifedipine , chemistry , divalent , biophysics , depolarization , contraction (grammar) , calcium , amiloride , voltage dependent calcium channel , intracellular , membrane potential , biochemistry , medicine , sodium , biology , organic chemistry
1 The effects of removal of extracellular divalent cations (experimental calcium paradox conditions) were studied on the whole‐cell current in freshly isolated smooth muscle cells (SMCs), and on contraction in rabbit aortic rings. 2 Aortic rings treated for 30–60 min with extracellular Ca 2+ ‐ and Mg 2+ ‐free solution contracted following readmission of extracellular Ca 2+ , even in the presence of nifedipine. 3 In isolated SMCs, the removal of extracellular Ca 2+ and Mg 2+ induced a non‐inactivating whole‐cell inward current and membrane depolarization. This current was a monovalent cation (MC) current which reversed at around 0 mV and conducted K + ≥ Cs + > Na + > Li + . Extracellular divalent cations (Ca 2+ , Mg 2+ , Ba 2+ , Mn 2+ and Ni 2+ ) inhibited MC current. 4 Using noise analysis of the whole‐cell MC current, the single MC channel conductance was estimated to be < 450 fS. 5 MC current was insensitive to nifedipine, TEA, 4‐aminopyridine, SK&F 96365 and S‐ nitroso‐ N‐ acetyl‐penicillamine (SNAP), but was decreased by amiloride and low pH. 6 When EGTA was present in Ca 2+ ‐ and Mg 2+ ‐free solution, a significant nifedipine‐sensitive Na + current through L‐type Ca 2+ channels developed in addition to MC current. 7 It is concluded that upon the removal of extracellular Ca 2+ and Mg 2+ from resting SMCs, an inward MC current develops allowing Na + influx and causing SMC depolarization which could be the important steps leading to vessel contraction upon Ca 2+ readmission. Addition of EGTA to Ca 2+ ‐ and Mg 2+ ‐free solution greatly potentiates Na + influx and vessel contraction by allowing additional Na + influx through L‐type Ca 2+ channels which are activated presumably by MC current‐induced depolarization.