: 17 L-typecalciumchannel;animals,laboratory;rats (atherosclerosis,as) ( Visualsonic ); ( ) 1.4, (vascularsmoothmusclecels,vsmcs),,,,,, 3.0%, 1L

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瑛离嵇
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1 16 ( ) JournalofNanchangUniversity(MedicalSciences)2018,Vol.58No.1 1, 1, 2 2, 2 2 1, (1., ; 2., ) : (SHR)Wistar,, 1.8~2.0mm, 5- (5-HT) A2 (U46619) -1(ET-1) ;L- (Cav1.2) (Nifedip- ine)(1μmol L -1 ), (P<0.05); Wistar, SHR (P<0.05); (1μmol L -1 ), (P<0.05) Wistar,SHR, L : ; ; ;L- ;, ; : R-332 : A : (2018) DOI: /j.cnki.ncdm ContractileFunctionofCoronaryArteriesin SpontaneouslyHypertensiveRats WU Qi 1,WANG Hao 1,DENGChun-yu 2,RAOFang 2, KUANGSu-juan 2,YANG Hui 2,XUJin-song 1 (1.Departmentof Vasculocardiology,theSecond Affiliated Hospitalof Nanchang University,Nanchang330006,China;2.Electrophysiology Group,Guangdong ProvincialInstituteof Cardiovascular Disease,Guangzhou510080,China) ouslyhypertensiveratsandnormalrats.methods ABSTRACT:Objective Toinvestigatethediferenceincoronaryconstrictionbetweenspontane- Thecoronaryarterieswereremovedfroma- dultspontaneouslyhypertensiveratsandnormalwistarratsundermicroscopetopreparethecor- onaryarteryringswithalengthof mm.thearterialringtensionwasdeterminedbyten- siometer.thechangesincoronaryarteryconstrictionwerestudiedbyusingdiferentagonists.re- sults Thetreatmentwith5-hydroxytryptamine(5-HT),thromboxane A2analogue U46619or endothelin-1(et-1)inducedaconcentration-dependentcontractionincoronaryarteries.theblood vesselcontractiontensionwassignificantlydecreasedafterincubationwithl-typecalciumchannel (Cav1.2)blockernifedipine(1μmol L -1 )(P<0.05).ComparedwithnormalWistarrats,ago- nists-inducedcoronaryconstrictionwasmarkedlyreducedinspontaneouslyhypertensiverats,es- pecialyafterincubationwithnifedipine(1μmol L -1 )(P<0.05).Conclusion Comparedwith normalwistarrats,spontaneouslyhypertensiveratsshowsignificantdecreaseinthecontractility ofcoronaryartery,which mayberelatedtotheatenuationofl-typecalciumchannelmediated contraction. KEY WORDS:spontaneouslyhypertensive;coronaryartery;vasoconstriction; : : ( ); (20161BAB205257) : (1992 ),,, :,, ; xujingsong@medmail.com.cn

2 : 17 L-typecalciumchannel;animals,laboratory;rats (atherosclerosis,as) ( Visualsonic ); ( ) 1.4, (vascularsmoothmusclecels,vsmcs),,,,,, 3.0%, 1L min MHz,5-,, (5-hydroxytryptamine,5-HT) -1 3 (endothelin-1,et-1) 3 [1] ;, (spontaneously (interventricularseptal hypertensiverats,shr) (KCl) systole,ivss) (interventricular (phenylephrine,pe) septaldiastole,ivsd) (left [2] ;, ventricularend-diastolicposterior walthickness, [3], LVPWd) (leftventricular, end-systolicposteriorwalthickness,lvpws), (leftventricularend-systolicinter-, SHR naldimension,lvids) (left, ventricular end-diastolic internal dimension, LVIDd) (leftventricularejection fraction,lvef) (CO 2 ), SPFWistarSHR,300~, 350g Wistar 4, :SCXK() SHR, (95%O 2+5%CO 2 ) K-H, :SCKK() , 1.2, 5-(5-hydroxytryptamine,5-HT),, A2 (9,11-dideoxy-11α,9α-epoxymetha-, nopros-taglandin,u46619) -1(Endothelin- 1.8~2.0 mm 1,ET-1) (Nifedipine) Sigma 40μm,, Nifedipine, DMSO, Krebs-Henseleit(K-H) (mmol L -1 ):NaCl119,NaHCO 325,MgCl 2,, 6H 2O1,KCl4.7,KH 2PO 41.2,CaCl 22.5,D-Glu- cose11.1; K-H (60mmol L -1 KCl): NaCl63.7,NaHCO 325,MgCl 2 6H 2O1,KCl60, [4-5] 5mL 37 K-H, 1.5 mn, 60min, 15min 1, KH 2PO 41.2,CaCl 22.5,D-Glucose mn, (95% O 2+5% CO 2 ),, ph ± , 95%O 2 5%CO 2 610M (DMT, );PowerLab8/30 (1.4.3 AD );DK-8D (, );StemiDV4 ( K-H K-H, ZEISS );Vevo2100, 5min, ( 4,

3 18 ( )20182,58 1 5min), 30min, (IVSd), (LVPWs) (LVPWd) 10% (P<0.01P<0.05), 1, 30 min, 1 100nmol L -1 SHR Wistar U46619, x±s 1μmol L -1 Ach, Wistar(n=6) SHR(n=6) 60%,,Ach SBPp/mmHg ± ±4.38 * *, 10%, DBPp/mmHg 85.20± ±8.60 * * [6] HR f/( min -1 ) ± ±13.87 IVSs/mm 2.19± ±0.46 IVSd/mm 1.31± ±0.17 * * 1.5 ± (mean±s.e.m) LVIDs/mm 4.81± ±0.43, LVIDd/mm 7.22± ±0.19 LVPWs/mm 2.24± ± %, / ; * LVPWd/mm 1.51± ±0.24 * * LVEF/% 62.05± ± %, / *P <0.05 * *P <0.01 Wistar,EC 50 1mmHg=0.133kPa 50%,pEC 50=-lg(EC 50 ) Prism HT SHR Wistar, Nifedipine lgec 50 (Emax) 5-HT(0.001~10μmol t,p<0.05 L -1 ), Wistar SHR 5-HT SHR - 2 Emax (P<0.001),2 pec50 (P>0.05) 2.1 SHR Wistar 5-HT SHR,SHR 1 2 (P<0.01);,SHR A:5-HT ;B:5-HT ;C: Nifedipine 5-HT ;D:Nifedipine 5-HT 1 L Nifedipine5-HT SHR/Wistar

4 : 19 2 pec50emax x±s Treatment pec50 Emax/% n Coronaryartery 5-HT(Wistar) 6.27± ± HT(SHR) 6.28± ±3.53 * * * 29 5-HT+1μmol L -1 nifedipine(wistar) 5.89± ± HT+1μmol L -1 nifedipine(shr) 5.54± ±8.65 * * * 17 U46619(Wistar) 7.37± ± U46619(SHR) 7.34± ±4.73 * * * 17 U μmol L -1 nifedipine(wistar) 6.55± ± U μmol L -1 nifedipine(shr) 6.35± ±3.56 * * * 10 *P<0.05 **P<0.01 ***P<0.001 Wistar 5-HT U46619 SHR -,L- nifedipine Emax (P <0.001),2 1μmol L min,nifedipine pec50 (P>0.05) 5-HT Wistar SHR U46619SHR 5-HT SHR Emax (P<0.001),2 pec50 (P>0.05), nifedipine1μmol L min 5-HT SHR,nifedipine U U46619 SHR Wistar U46619 SHR - Nifedipine U46619(0.001~1μmol L -1 ), Wistar SHR U46619 Wistar SHR Emax (P<0.001),2pEC50 (P>0.05) SHR 2 2 A:U46619 ;B:U46619 ;C:Nifedipine U46619 ;D:Nifedipine U L NifedipineU46619 SHR/Wistar

5 ET-1 SHR Wistar ET-1 Nifedipine ET-1(0.001~0.03μmol L -1 ), Wistar SHR WistarSHR,,ET-1 SHR,ET-1 SHR Wistar (P<0.05) (P<0.05) 3 3 ( )20182,58 1, nifedipine1μmol L min,nifedipine ET-1 3 A:ET-1 ;B:ET-1 ;C: Nifedipine ET-1 ;D:Nifedipine 3 L NifedipineET-1 SHR/Wistar 5-HT U46619 ET-1 Wistar, [8] U46619 A2 (TP), TP SHR, A2 ;L- (1μmol L -1 ) [9], ET-1, ;Wistar,,SHR, ;, SHR, SHR Wistar VSMC, (phosphatidylinositol bi-,ca 2+, sphosphate,pip2) (inositol [10] Ca 2+ triphosphate,ip3) (diacylglycerol,, DAG) IP3, Ca 2+, Ca 2+ [7],,, VSMC,5-HT,

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