中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2012年
2期
157-160
,共4页
李其勇%姜荣建%舒燕%孔洪%赖金川%程标
李其勇%薑榮建%舒燕%孔洪%賴金川%程標
리기용%강영건%서연%공홍%뢰금천%정표
冠状血管%大电导钙激活钾通道%利钠肽,脑%膜片钳术
冠狀血管%大電導鈣激活鉀通道%利鈉肽,腦%膜片鉗術
관상혈관%대전도개격활갑통도%리납태,뇌%막편겸술
Coronary vessels%Large-conductance calcium-activated potassium channels%Natriuretic peptide,brain%Patch-clamp techniques
目的 探讨利钠肽C受体( NPR-C)和大电导钙激活钾通道(BKCa)在B型利钠肽(BNP)舒张猪冠状动脉中的作用.方法 取健康成年家猪冠状动脉,血管张力实验随机分为BNP组、cANF4-28+ BNP组和TEA+ BNP组,每组均含10个血管段,观察BNP对猪冠状动脉的舒张作用及NPR-C阻断剂cANF4-28、BKCa阻断剂四乙铵(TEA)预处理后BNP舒血管效应的变化.全细胞膜片钳实验随机分为对照组、BNP组、TEA组和TEA+ BNP组,观察各种干预措施对BKCa电流密度的影响,每组均含10个细胞数.结果 BNP组血管最大舒张率为(68.51±11.50)%,cANF4-28+ BNP组最大舒张率为(65.67±11.90)%,两组间差异无统计学意义(P>0.05).TEA+ BNP组最大舒张率为(28.87±4.55)%,低于BNP组,差异有统计学意义(P<0.05).当钳制电位在+60 mV时,BNP组的电流密度为( 78.48±5.86) pA/pF,高于对照组的电流密度(53.84±4.55) pA/pF,差异有统计学意义(P<0.05).TEA组和TEA+ BNP组的电流密度分别为(28.80±2.76)pA/pF和(30.60±3.88)pA/pF,两组间差异无统计学意义(P>0.05),两组的电流密度均低于对照组,差异均有统计学意义(P均<0.05).结论 BNP能通过激活BKCa对猪冠状脉平滑肌产生舒张作用,NPR-C未参与其中.
目的 探討利鈉肽C受體( NPR-C)和大電導鈣激活鉀通道(BKCa)在B型利鈉肽(BNP)舒張豬冠狀動脈中的作用.方法 取健康成年傢豬冠狀動脈,血管張力實驗隨機分為BNP組、cANF4-28+ BNP組和TEA+ BNP組,每組均含10箇血管段,觀察BNP對豬冠狀動脈的舒張作用及NPR-C阻斷劑cANF4-28、BKCa阻斷劑四乙銨(TEA)預處理後BNP舒血管效應的變化.全細胞膜片鉗實驗隨機分為對照組、BNP組、TEA組和TEA+ BNP組,觀察各種榦預措施對BKCa電流密度的影響,每組均含10箇細胞數.結果 BNP組血管最大舒張率為(68.51±11.50)%,cANF4-28+ BNP組最大舒張率為(65.67±11.90)%,兩組間差異無統計學意義(P>0.05).TEA+ BNP組最大舒張率為(28.87±4.55)%,低于BNP組,差異有統計學意義(P<0.05).噹鉗製電位在+60 mV時,BNP組的電流密度為( 78.48±5.86) pA/pF,高于對照組的電流密度(53.84±4.55) pA/pF,差異有統計學意義(P<0.05).TEA組和TEA+ BNP組的電流密度分彆為(28.80±2.76)pA/pF和(30.60±3.88)pA/pF,兩組間差異無統計學意義(P>0.05),兩組的電流密度均低于對照組,差異均有統計學意義(P均<0.05).結論 BNP能通過激活BKCa對豬冠狀脈平滑肌產生舒張作用,NPR-C未參與其中.
목적 탐토리납태C수체( NPR-C)화대전도개격활갑통도(BKCa)재B형리납태(BNP)서장저관상동맥중적작용.방법 취건강성년가저관상동맥,혈관장력실험수궤분위BNP조、cANF4-28+ BNP조화TEA+ BNP조,매조균함10개혈관단,관찰BNP대저관상동맥적서장작용급NPR-C조단제cANF4-28、BKCa조단제사을안(TEA)예처리후BNP서혈관효응적변화.전세포막편겸실험수궤분위대조조、BNP조、TEA조화TEA+ BNP조,관찰각충간예조시대BKCa전류밀도적영향,매조균함10개세포수.결과 BNP조혈관최대서장솔위(68.51±11.50)%,cANF4-28+ BNP조최대서장솔위(65.67±11.90)%,량조간차이무통계학의의(P>0.05).TEA+ BNP조최대서장솔위(28.87±4.55)%,저우BNP조,차이유통계학의의(P<0.05).당겸제전위재+60 mV시,BNP조적전류밀도위( 78.48±5.86) pA/pF,고우대조조적전류밀도(53.84±4.55) pA/pF,차이유통계학의의(P<0.05).TEA조화TEA+ BNP조적전류밀도분별위(28.80±2.76)pA/pF화(30.60±3.88)pA/pF,량조간차이무통계학의의(P>0.05),량조적전류밀도균저우대조조,차이균유통계학의의(P균<0.05).결론 BNP능통과격활BKCa대저관상맥평활기산생서장작용,NPR-C미삼여기중.
Objective To investigate the role of C-type natriuretic peptide receptor (NPR-C) and large-conductance calcium-activated potassium channels ( BKCa ) in brain natriuretic peptide (BNP) induced porcine coronary artery dilation.Methods 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 + BKCa blocker tetraethylammonium (TEA, 1 mmol/L). The vascular tone experiments were observed on 10 vessel segments. BKCa current density was measured by the whole-cell patch clamp technique.Results 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 mY,the BKCa 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 ].Conclusion BNP could relax the porcine coronary arterial smooth muscles by increasing BKca current,and this effect is not mediated by NPR-C.