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Objective: to investigate the regulation in vascular tension of diabetic coronary artery by large conductance Ca(2+)-activated K(+) channel (BK channel) and to elucidate the mechanisms of coronary dysfunctions due to diabetes., Methods: regulation of vascular tension in normal coronary artery was evaluated by videomicroscopy system. Streptozotocin-induced rat diabetic animal model was established successfully by intraperitoneal injection. Coronary smooth muscle cells were isolated by enzyme digestion. The BK currents in control and diabetic groups were recorded by patch clamp technique in whole cell configuration. Changes of vascular tension in normal and diabetic coronary arteries were assayed by multi-wire myograph system., Results: more than 50% was contracted in inner diameters of coronary arteries when 100 nmol/L IBTX, a specific BK channel blocker, was applied. In comparison with normal group, the BK current densities in diabetic group significantly decreased when test potentials were more than 60 mV (P < 0.05). The BK current densities at 150 mV in normal group and diabetic group were (275 ± 40) pA/pF and (70 ± 10) pA/pF respectively. When 100 mmol/L KCl was washed out, vascular tensions of normal and diabetic coronary artery were (398 ± 38) mg and (390 ± 35) mg respectively (P > 0.05); however, when 100 nmol/L IBTX was added, the vascular tensions of normal and diabetic coronary artery were (395 ± 40) mg and (50 ± 7) mg (P < 0.05)., Conclusion: BK channels play an important role in the regulation of coronary vascular tension, whereas BK channels in diabetic coronary artery are dysfunction, BK currents decrease and vascular tensions increase.

Objective: To investigate the role of P-type Na+ -K+ -ATPase in the mechanism of migraine., Methods: nitroglycerin induced migraine Twenty Sprague-Dawley rats, 10 male and 10 female, were randomly divided into 2 groups: model group, undergoing subcutaneous injection of nitroglycerin 10 mg/kg once a week for 4 weeks so as to establish migraine model, and control group, undergoing subcutaneous injection of normal saline. Then the rats were killed with their trigeminal ganglia, trigeminocervical complex, and cortex of frontal lobe taken out. RT-PCR and Western-blotting were used to detect the mRNA and protein expression of P-type Na+ -K+ -ATPase. Immuno-precipitation assay was conducted to observe the Na+ -K+ -ATPase activity. The concentration of intracellular Ca2+ was investigated by Fluo-3/AM fluorometric method., Results: The mRNA and protein expression levels and activity of P-type Na+ -K+ -ATPase in the trigeminal ganglion and trigeminocervical complex of the model group were 0.72 +/- 0.05, 0.59 +/- 0.05, and 5.21 +/- 0.51 respectively, and the mRNA and protein expression levels and activity of P-type Na+ -K+ -ATPase in the cortex of frontal lobe of the model group were 0.70 +/- 0.05, 0.60 +/- 0.05, and 3.61 +/- 0.49 respectively, all significantly lower than those of the control group (0.83 +/- 0.10, 0.67 +/- 0.06, 6.53 +/- 0.73, 0.81 +/- 0.08, 0.71 +/- 0.09, and 6.61 +/- 0.73 respectively, all P < 0.05). The concentration of intracellular Ca2 in trigeminal ganglion and trigeminocervical complex and the concentration of Ca2+ in the cortex of frontal lobe of the model group were 211,182 +/- 12,973 and 186,511 +/- 18,297 respectively, both significantly higher than those of the control group (135,243 +/- 18,105 and 143,289 25,175 respectively, both P < 0.01)., Conclusion: P-type Na+ -K+ -ATPase may infect the pathogenesis of migraine by its expression and activity.