Yu Jun, Zhu Miao-Zhang, Liu Li-Bing, Chen Bao-Ying, Lu Shun-Yan, Zhou Jing-Jun, Fu Zhao-Jun
Experiment Teaching Center, Tangdu Hospital, Xi'an, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2006 Feb;22(1):94-7.
To investigate effect and mechanism of vasonatrin peptide (VNP) on Ca2+ activated K+ channels (K(Ca)) of vascular smooth muscle cells (VSMCs) isolated from rat mesentery arteries.
Changes of K(Ca) induced by VNP were measured by the means of whole cell recording mode of patch clamp, furthermore effects of HS-142-1(0.3 g/L), 8-Br-cGMP and methylene blue (MB) were observed.
K(Ca) was significantly enhanced by VNP (10(-6) mol/L), which was mimicked by 8-Br-cGMP(10(-3) mol/L) and blocked completely by HS-142-1 or MB (2 x 10(-5) mol/L).
VNP increases K(Ca) of VSMCs isolated from rat mesenteric arteries, by binding with natriuretic peptide guanylate cyclase-coupled receptors and increasing the intracellular level of cGMP in VSMCs.
研究血管钠尿肽（VNP）对大鼠肠系膜动脉血管平滑肌细胞（VSMCs）钙激活钾通道（K（Ca））的作用及其机制。
采用膜片钳全细胞记录模式检测VNP诱导的K（Ca）变化，并观察HS-142-1（0.3 g/L）、8-溴环磷酸鸟苷（8-Br-cGMP）和亚甲蓝（MB）的作用。
VNP（10^-6 mol/L）可显著增强K（Ca），8-Br-cGMP（10^-3 mol/L）可模拟该作用，HS-142-1或MB（2×10^-5 mol/L）可完全阻断该作用。
VNP通过与利钠肽鸟苷酸环化酶偶联受体结合，增加VSMCs内cGMP水平，从而增加大鼠肠系膜动脉VSMCs的K（Ca）。
