Li Qi-yong, Jiang Rong-jian, Shu Yan, Kong Hong, Lai Jin-chuan, Cheng Biao
Department of Cardiology, Sichuan Academy of Medical Sciences, Chengdu, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2012 Feb;40(2):157-60.
To investigate the role of C-type natriuretic peptide receptor (NPR-C) and large-conductance calcium-activated potassium channels (BK(Ca)) in brain natriuretic peptide (BNP) induced porcine coronary artery dilation.
Porcine coronary artery rings were obtained and treated with BNP (10(-6) mol/L), BNP + NPR-C antagonist cANF4-28 (10(-6) mol/L) and BNP + BK(Ca) blocker tetraethylammonium (TEA, 1 mmol/L). The vascular tone experiments were observed on 10 vessel segments. BK(Ca) current density was measured by the whole-cell patch clamp technique.
The maximum diastolic rate was similar between BNP group (68.51% ± 11.50%) and cANF4-28 + BNP group (65.67% ± 11.90%, P > 0.05) while significantly reduced in TEA + BNP group (28.87% ± 4.55%, all P < 0.05). When the holding potential was set at +60 mV, the BK(Ca) current density of BNP group was (78.48 ± 5.86) pA/pF, which was significantly higher than control group [(53.84 ± 4.55) pA/pF, P < 0.05], which was equally reduced in the TEA group and TEA + BNP group [(28.80 ± 2.76) pA/pF and (30.60 ± 3.88) pA/pF respectively, all P < 0.05 vs. control group].
BNP could relax the porcine coronary arterial smooth muscles by increasing BK(Ca) current, and this effect is not mediated by NPR-C.
研究C型利钠肽受体（NPR-C）和大电导钙激活钾通道（BK(Ca)）在脑钠肽（BNP）诱导的猪冠状动脉舒张中的作用。
获取猪冠状动脉环，分别用BNP（10⁻⁶ mol/L）、BNP + NPR-C拮抗剂cANF4-28（10⁻⁶ mol/L）和BNP + BK(Ca)阻滞剂四乙铵（TEA，1 mmol/L）处理。对10个血管节段进行血管张力实验观察。采用全细胞膜片钳技术测量BK(Ca)电流密度。
BNP组（68.51% ± 11.50%）与cANF4-28 + BNP组（65.67% ± 11.90%，P > 0.05）的最大舒张率相似，而TEA + BNP组显著降低（28.87% ± 4.55%，所有P < 0.05）。当钳制电位设置为 +60 mV时，BNP组的BK(Ca)电流密度为（78.48 ± 5.86）pA/pF，显著高于对照组[（53.84 ± 4.55）pA/pF，P < 0.05]，TEA组和TEA + BNP组均降低[分别为（28.80 ± 2.76）pA/pF和（30.60 ± 3.88）pA/pF，与对照组相比所有P < 0.05]。
BNP可通过增加BK(Ca)电流使猪冠状动脉平滑肌舒张，且此作用不受NPR-C介导。
