ABSTRACT
To explore the relation between the gene polymorphism of type 2 diabetes patients and their response to sulphonylurea(SU) and accomplish the personal therapy,the range of the SU pharmacogenomics should includes genes involved in the process of SU metabolism and acting,other pathological or physiological process of type 2diabetes also should be investigated,the genes recoding sulphonylurea receptor 1(SUR1),inwardly rectifying K+ channels 6.2(Kir6.2),CYP2C9 and insulin receptor substrate 1(IRS1) are the most important.
ABSTRACT
To identify the presence of inwardly rectifying K+ channels and its characteristics, membrane currents were measured using a whole-cell patch clamp from isolated gastric myocytes of guinea-pig. Change of external K+ concentration from 5 to 90 mM induced an inward current at a holding potential of 80 mV. The high K+-induced inward current was blocked by Ba2+ and Cs+, but not by glibenclamide. With 90 mM K+ in bath, the Ba2+- and Cs+-sensitive currents showed strong inward rectification. Ten mM TEA weakly blocked the inward current only at potentials more negative than 50 mV. With 90 mM K+ in bath, hyperpolarizing step pulses from 10 mV induced inward currents, which were inactivated at potentials more negative than 70 mV. Reduction of external K+ to 60 mM decreased the amplitudes of the currents and shifted the reversal potential to more negative potential. The inactivation of inward K+ current at negative clamp voltage was not affected by removing external Na . These results suggest that the inwardly rectifying K+ channels may exist in gastric smooth muscle.