Abstract

Objective To study the electrophysiology and pharmacology of voltage-dependent calcium channels (VDCCs) currents in cerebral artery myocytes of rats specifically to help for related arterial physiology or pathology research.Methods Myocytes were isolated enzymatically and patch clamp was used to test the resting potential and VDCCs currems in whole model,as well as effects of extracellular divalent cations concentration and Nifedipine on VDCCs currents.Results The resting potential was (50.42 ±0.26) mV,step protocol at 10 mV and ramp protocol at (9.80±0.92) mmol/L elicited maximum VDCCs currents density in (-5.22±0.51)pA/pF and (-4.89 ±0.65) pA/pF (10 mmol/L BaCl2).The maximum VDCCs currents consisted of high-voltage activation (HVA) VDCCs exclusively (P =0.17),however,denying the existence of low-voltage activation (LVA) VDCCs currents.Furthermore,the VDCCs currents density correlated with extracellular Ba2+ concentration positively (P < 0.05),and of the VDCCs currents,Nifedipine was able to inhibit 86.13 0.76% maximally with the IC50 6.02 mmol/L Conclusions Our study confirmed that HVA-VDCCs accounted for all the VDCCs currents and Nifedipine-insensitive calcium currents (NICCs) in cerebral artery myocytes of rats.Accordingly,further studies in term of ion channel (s) accounting for NICCs and its significance for myogenic tone of cerebral artery and cerebral autoregulation are required. Key words: Cerebral arteries; Voltage-dependent calcium channels; Patch clamp

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