钾通道在D型钠尿肽抑制胃动力中的作用

目的:探讨钾通道在D型钠尿肽抑制豚鼠胃窦环形肌自发性收缩活动中的作用.方法:采用四道生理记录仪记录豚鼠胃窦环形肌自发性收缩活动;应用放射免疫法测定豚鼠胃窦环形肌组织和灌流液中环-磷酸鸟苷(cGMP)含量;运用全细胞模式的膜片钳技术记录豚鼠胃窦环形肌上钙敏感钾电流和延迟整流型钾电流.结果:DNP抑制豚鼠胃窦环形肌自发性收缩活动并呈现剂量依赖性.1、10、100及1000nmol/L的DNP抑制自发性收缩幅度分别为35%±6%、54%±6%、78%±13%及94%±6%.10 nmol/L鸟苷酸环化酶抑制剂LY83583使收缩幅度抑制减弱(42%±6%vs60%±4%.P<0.05);而用100 nm01/L的cGMP依赖的磷酸脂酶抑制剂zaparinast使DNP对胃窦环行肌自发性收缩的抑制效应增强(72%±7%vs58%±5%,P<0.05).DNP明显增加豚鼠胃窦环形肌组织和灌流液中的cGMP水平.10 nmol/LDNP增加豚鼠胃窦环形肌上钙敏感钾电流,在60mV时增加的幅值为62.31%±3.22%,抑制延迟整流型钾电流,在60 mV时抑制幅度为18%±2.3%.结论:DNP通过增加I<,K(ca)>和cGMP途径实现对豚鼠胃窦环形肌的舒张作用.I<,K(v)>不参与此过程,但在维持豚鼠胃窦环形肌细胞的静息膜电位中起重要作用.     

NP-cGMP-PKG信号通路在D型钠尿肽抑制延迟整流型钾电流中的作用

目的:探讨NP-cGMP-PKG信号通路在D型钠尿肽(DNP)抑制豚鼠胃窦环形肌细胞上延迟整流型钾电流中的作用及其相关机制.方法:用全细胞模式的膜片钳技术记录豚鼠胃窦环形肌上延迟整流型钾电流(IK(V)).并观察NP-cGMP-PKG信号通路在DNP抑制豚鼠胃窦环形肌细胞上延迟整流型钾电流中的作用.结果:DNP抑制豚鼠胃窦环形肌上IK(V)并呈现剂量依赖关系.0.01,0.1和1 μmol/L的DNP在去极化到60 mV时使IK(V)抑制到原来的83.5%±2.1%,71.8%±2.3%和63.8%±2.2%.鸟苷酸环化酶抑制剂LY83583减弱这种抑制作用,0.1μmol/L的LY83583使1 μmol/L的DNP抑制IK(V)的程度由原来抑制到63.8%±2.2%减弱为抑制到76.8%±2.3%.而cGMP敏感的磷酸酯酶抑制zaparinast却能增强这种作用.1 μmol/L的zaparinast使1 μmol/L的DNP抑制IK(V)的程度由原来抑制到63.8%±2.2%增强为抑制到56.8%±2.1%.DNP对IK(V)的抑制作用可完全被cGMP依赖的蛋白激酶G(PKG)抑制剂KT5823所消除,但不受cGMP依赖的蛋白激酶A(PKA)抑制剂的影响.结论:NP-cGMP-PKG途径参与DNP抑制豚鼠胃窦环形肌细胞上IK(V)过程,而cAMP-PKA途径并不参与此过程.IK(V)在维持豚鼠胃窦环形肌细胞静息电位中起重要作用.     

钙离子在CNP抑制Ach增强胃窦环行平滑肌收缩效应中的作用

目的 探讨细胞内外钙离子在C型钠尿肽(CNP)对乙酰胆碱(Ach)引起的大鼠离体胃窦环行平滑肌收缩效应中的作用.方法 利用浴槽孵育离体大鼠胃窦环行肌肌条,用离体平滑肌张力记录装置记录平滑肌肌条收缩活动,观察钙离子对Ach引起的大鼠离体胃窦环行平滑肌收缩效应的影响.结果 CNP对Ach引起的胃平滑肌自发性收缩增强效应有明显的抑制作用,在用无钙灌流液灌流后,CNP仍能抑制Ach引起的收缩效应.而用胞内钙离子释放抑制剂(TMB-8)后,CNP不能抑制Ach引起的收缩效应.结论 CNP抑制Ach引起的胃平滑肌自发性收缩增强效应与胞内钙释放有关.     

大黄素对豚鼠胃窦环形肌自发性收缩活动的影响及相关机制

目的:观察大黄素(emodin)对豚鼠胃窦环形肌自发性收缩活动的影响及相关机制.方法:用四道生理记录仪记录豚鼠胃窦环形肌自发性收缩活动;用膜片钳记录豚鼠胃窦环形肌细胞上L型钙电流,观察L型钙电流在大黄素增强豚鼠胃窦环形肌自发性收缩活动中的作用.结果:大黄素在一定的浓度范围内增强豚鼠胃窦环形肌自发性收缩活动并呈剂量依赖性,给予5、10、15、20、25、50mol/L的大黄素后豚鼠胃窦环形肌自发性收缩的幅度分别为对照组的108.2%±6.2%、150.6%±8.3%、198.2%±7.6%、200.2%±8.6%、160.0%±6.8%、81.2%±6.2%.预先加入10mol/L的硝苯地平,完全阻断大黄素增强豚鼠胃窦环形肌自发性收缩活动.10mol/L和20mol/L的大黄素明显增强豚鼠胃窦环形肌细胞上钡电流(IBa),用10mol/L的大黄素灌流开始后200s左右时IBa电流峰值变化趋于稳定,20mol/L的大黄素灌流开始后170s左右时IBa电流峰值变化趋于稳定.加药后IBa电流峰值分别增加到对照组电流最大值的137.88%±5.79%和158.69%±6.11%.结论:大黄素增强豚鼠胃窦环形肌自发性收缩,细胞外钙通过L型钙通道内流入细胞内引起平滑肌收缩是大黄素促进豚鼠胃窦环形肌自发性收缩的作用机制之一.     

P2X受体对豚鼠胃窦环行肌自发性收缩运动的影响

目的:探讨P2X受体激动剂α,β-methylene ATP (α,β-MeATP)对豚鼠胃窦环行肌运动的影响及其离子通道机制.方法:采用EWG/B豚鼠,制备去黏膜胃窦环行肌条(10×1.5 mm),并将其固定于恒温灌流槽内(37℃),用碳酸氢钠缓冲液连续灌流并通氧(950 mL/L O_2,50 mL/L CO_2).利用SMUP-E生物信号处理系统记录胃窦平滑肌自发性收缩活动,Ⅱ型胶原酶消化法分离豚鼠胃窦环行肌单细胞,传统全细胞膜片钳技术记录急性分离的胃窦平滑肌细胞膜电位和离子电流,包括钙激活钾电流、延迟整流型钾电流及电压依赖性钙电流.结果:嘌呤能P2X受体激动剂α,β-MeATP明显抑制豚鼠胃窦环行肌自发性收缩,并有明显的量效倚赖关系:5,10,20,40,100μmol/Lα,β-MeATP作用下,环行肌收缩幅度分别由对照组的100%下降到90%±2%.81%±4%,68%±4%,59%±7%和29%±4%(P<0.05).用神经阻断剂Tetrodotoxin (TTX)预处理后,α,β-MeATP对胃窦环行肌自发性收缩的抑制作用仍不受影响;在传统全细胞膜片钳电流钳模式下,500μmol/Lα,β-MeATP不影响细胞膜电位,也对两种外向钾电流,即延迟整流型钾电流和钙激活钾电流没有影响;不同浓度的α,β-MeATP对电压依赖性钙电流没有影响.结论:P2X受体激动剂抑制豚鼠胃窦环行肌自发性收缩,其作用机制不依赖内在神经,也不依赖细胞膜离子通道以及膜电位改变.     

CNP对糖尿病大鼠胃窦环形肌自发性收缩的影响

目的探讨C型钠尿肽（CNP）对糖尿病大鼠胃窦环形肌自发性收缩的影响及其机制。方法取大鼠24只随机分为对照组和糖尿病组,用链脲佐菌素建立糖尿病模型,4周后制备胃窦环形肌条,肌条收缩活动稳定后,分别加入不同浓度CNP（1×10^-8、3×10^-8、1×10^-7mol/L）,均采用多道生理信号采集处理系统计算CNP致平滑肌张力的抑制率,用放射免疫分析法测定胃平滑肌组织中环鸟苷酸（cGMP）浓度。结果与对照组相比,糖尿病组CNP对胃窦环形平滑肌张力的抑制率明显增加,并有浓度依赖性（P〈0.05,〈0.01）,平滑肌细胞内cGMP浓度明显增高（P〈0.05）。结论CNP可抑制糖尿病大鼠胃窦环形肌的收缩,此作用与其促使cGMP的浓度增高有关。     

糖尿病胃动力障碍大鼠胃窦平滑肌组织中CNP和NPR-B蛋白含量变化

目的探讨糖尿病胃动力障碍大鼠胃窦平滑肌组织中C型钠尿肽（CNP）和B型钠尿肽受体（NPR-B）的蛋白含量变化。方法腹腔注射链脲佐菌素（STZ）（65 mg/kg）4周,制备糖尿病动物模型。利用多道生理信号记录系统记录糖尿病大鼠胃窦平滑肌收缩活动,将发生胃窦平滑肌收缩活动紊乱的大鼠列入糖尿病胃动力障碍模型。采用免疫组织化学方法观察糖尿病大鼠胃窦平滑肌中CNP和NPR-B的分布。结果糖尿病胃动力障碍组大鼠与正常对照组相比胃窦平滑肌组织CNP表达无明显差异,但NPR-B表达明显增多（P〈0.01）。结论糖尿病大鼠发生胃动力障碍可能与胃窦平滑肌中NPR-B上调有关,提示糖尿病大鼠胃CNP-NPR-B/pGC-cGMP转导系统的改变可能参与胃动力障碍的发生。     

ANP与5-HT在胃肠道中的定位及相互关系的研究

自1981年发现心房钠尿肽（ANP）以来,目前钠尿肽（NP）家族已有六大成员,即ANP、BNP、CNP、DNP、VNP、MNP。NP家族成员共同的结构特征是由17个氨基酸组成环形结构,其共有的生理学作用是利尿、利钠、舒张血管、降低血压和调节电解质平衡。Vuolteenaho等首次在大鼠的胃和小肠内发现ANP的免疫反应物质,以后相继在大鼠的大肠,豚鼠的胃、小肠、结肠以及人的胃、空肠、回肠、结肠和直肠等组织中也发现有ANP的免疫反应物质,并在大鼠的小肠微绒毛、空肠、回肠上皮细胞中发现ANP受体。随着研究的深入,人们发现胃肠道中5-羟色胺（5-HT）和ANP有密不可分的关系。现将其研究现状综述如下。     

N受体对四磨汤诱发的胃窦平滑肌收缩的影响

目的研究烟碱（N）受体对四磨汤诱发的sD大鼠离体胃窦平滑肌条收缩活动的影响。方法离体胃窦平滑肌条置于盛有Krebs液的组织浴槽中以记录其等长收缩活动,观察不同剂量四磨汤（1μL、5μL、25μL、50μL、100μL、150μL、200μL）对大鼠胃窦平滑肌条收缩活动的影响,并观察N受体阻断剂六烃季胺（10^-4mol／L）对四磨汤引起的胃窦平滑肌收缩活动的影响。结果四磨汤引起大鼠胃窦纵行和环行平滑肌条收缩活动增加呈剂量依赖性。六烃季胺对于四磨汤引起的胃窦纵、环形平滑肌条兴奋作用均具有部分抑制效应,对环行肌条的作用明显高于对纵行肌的影响。结论四磨汤对大鼠胃窦平滑肌的收缩活动具有明显的兴奋作用,但部分作用与N受体有关,胃窦环行肌更为依赖N受体的作用。     

莱菔子对豚鼠体外胃窦环行肌条收缩活动的影响

[目的]观察莱菔子水煎剂对豚鼠体外胃窦环行肌条的收缩活动并探讨其作用机制。[方法]将胃窦环行肌条置于灌流肌槽内,采用累积加莱菔子和分别加阻断剂的方法,观察其对肌条收缩活动的影响。[结果]莱菔子增大胃窦环行肌条的收缩波平均振幅及其收缩频率,并呈一定剂量依赖关系,M3胆碱能受体拮抗剂4-DAMP可部分阻断其振幅的增大。[结论]莱菔子水煎剂增大豚鼠胃窦环行肌条收缩波平均振幅的作用可能部分经由兴奋胆碱能M3受体而不是胆碱能M2受体。     

Role of calcium-activated potassium currents in CNP-induced relaxation of gastric antral circular smooth muscle in guinea pigs

AIM: To investigate ion channel mechanism in CNP-induced relaxation of gastric circular smooth muscle in guinea pigs.METHODS: Spontaneous contraction of gastric smooth muscle was recorded by a four -channel physiograph. The whole cell patch-damp technique was used bo record calcium-activated potassium currents and membrane potential in the gastric myocytes isolated by collagenase.RESULTS: C-type natriuretic peptide (CNP) markedly inhibited the spontaneous contraction in a dose-dependent manner in gastric circular smooth muscle in guinea pigs.Ly83583, an inhibitor of guanylate cyclase, weakened CNP-induced inhibition on spontaneous contraction but Zaparinast, an inhibitor of cGMP sensitive phosphoesterase,potentiated CNP-induced inhibition in gastric circular smooth muscles. The inhibitory effects of CNP on spontaneous contraction were blocked by tetrathylammonium (TEA), a nonselective potassium channel blocker. CNP hyperpolarized membrane potential from -60.0 mV&#177;2.0 mV to -68.3 mV&#177;3.0 mV in a single gastric myocyte. CNP increased calcium-activated potassium currents (IK（ca)) in a dose-dependent manner in gastric circular myocytes. CNP also increased the spontaneously transient outward currents(STOCs). Ly83583 partly blocked CNP-induced increase of calcium-activated potassium currents, but Zaparinast potented the effect.CONCLUSION:CNP inhibits spontaneous contraction,and potassium channel may be involved in the process in gastric circular smooth muscle of guinea pigs.CNP-induced increase of IK(ca) mediated by a cGMP dependent pathway.     

Dendroaspis natriuretic peptide relaxes gastric antral circular smooth muscle of guinea-pig through the cGIvlP/cGMP-dependent protein kinase pathway

AIM: To systematically investigate if cGMP/cGMPdependent protein kinase G (PKG) signaling pathway may participate in dendroaspis natriuretic peptide (DNP)-induced relaxation of gastric circular smooth muscle.METHODS: The content of cGMP in guinea pig gastric antral smooth muscle tissue and perfusion solution were measured using radioimmunoassay,spontaneous contraction of gastric antral circular muscles recorded using a 4-channel physiograph; and Ca2 -activated K currents (Ik(Ca)and spontaneous transient outward currents (STOCs) in isolated gastric antral myocytes were recorded using the whole-cell patch clamp technique.]RESULTS: DNP markedly enhanced cGMP levels in gastric antral smooth muscle tissue and in the perfusion medium.DNP induced relaxation in gastric antral circular smooth muscle,which was inhibited by KT5823,a cGMP-dependent PKG inhibitor.DNP increased IK(Ca)* This effect was almost completely blocked by KT5823,and partially blocked by LY83583,an inhibitor of guanylate cyclase to change the production of cGMP.DNP also increased STOCs.The effect of DNP on STOCs was abolished in the presence of KT5823,but not affected by KT-5720,a PKA-specific inhibitor.CONCLUSION: DNP activates IK(Ca) and relaxes guinea-pig gastric antral circular smooth muscle via the cGMP/PKG-dependent singling axis instead of cAMP/PKA pathway.     

Dendroaspis natriuretic peptide relaxes gastric antral circular smooth muscle of guinea-pig through the cGMP/cGMP-dependent protein kinase pathway

AIM： To systematically investigate if cGMP/cGMPdependent protein kinase G （PKG） signaling pathway may participate in dendroaspis natriuretic peptide （DNP）-induced relaxation of gastric circular smooth muscle.
METHODS： The content of cGMP in guinea pig gastric antral smooth muscle tissue and perfusion solution were measured using radioimmunoassay; spontaneous contraction of gastric antral circular muscles recorded using a 4-channel physiograph; and Ca^2＋-activated K^＋ currents （IK（Ca）） and spontaneous transient outward currents （STOCs） in isolated gastric antral myocytes were recorded using the whole-cell patch clamp technique.
RESULTS： DNP markedly enhanced cGMP levels in gastric antral smooth muscle tissue and in the perfusion medium. DNP induced relaxation in gastric antral circular smooth muscle, which was inhibited by KT5823, a cGMP-dependent PKG inhibitor. DNP increased IK（Ca）. This effect was almost completely blocked by KT5823, and partially blocked by LY83583, an inhibitor of guanylate cyclase to change the production of cGMP. DNP also increased STOCs. The effect of DNP on STOCs was abolished in the presence of KT5823, but not affected by KT-5720, a PKA-specific inhibitor.
CONCLUSION： DNP activates IK（ca） and relaxes guinea-pig gastric antral circular smooth muscle via the cGMP/PKG-dependent singling axis instead of cAMP/ PKA pathway.     

Comparative study in the effect of C-type natriuretic peptide on gastric motility in various animals

AIM: To investigate the effect of natriuretic peptides on gastric motility in various animals, and the effect of C-type natriuretic peptide (CNP) on spontaneous contraction of gastric smooth muscle in rat, guinea-pig and human in vitro was compared.METHODS: Spontaneous contraction of gastric smooth muscle was recorded by four channel physiograph.RESULTS: In the guinea-pig and rat gastric antral circular smooth muscle, CNP markedly decreased the amplitude of spontaneous contraction but it didn't affect the frequency,however, the contractile activity was completely inhibited by CNP in gastric antral longitudinal smooth muscle. In the human gastric antral circular and longitudinal smooth musie, CNP completely inhibited spontaneous contraction. In the circular smooth muscle of guinea-pig and rat gastric fundus,CNP obviously decreased the amplitude of spontaneous contraction but it didn't affect the frequency, however, the contractile activity was completely inhibited by CNP in smooth muscle of fundus longitudinal. In the circular and longitudinal smooth muscle of guinea-pig gastric body, CNP at first induced a relaxation and then an increase in amplitude of spontaneous contraction (rebound contraction), but the frequency was not changed. After the circular smooth muscle of gastric body was pretreated with atropine, an M receptor blocker, the rebound contraction was abolished; In circular and longitudinal smooth muscle of rat gastric body, CNP induced a transient and slight relaxation and successively followed by the recovery in amplitude of spontaneous contraction but it also didn't affect the frequency. After the smooth muscle was pretreated with atropine, the transient and slight relaxation was replaced by long term and complete inhibition; The percentage of CNP-induced inhibition was 76.77±6.21% (fundus), 67.21±5.32 % (body) and 58.23±6.21% (antral) in the gastric circular muscle, however, the inhibitory percentage was 100±0.00 % (fundus), 68.66±3.55 % (body) and 100±0.00 % (antrum) in the gastric longitudinal smooth muscle of guinea-pigs; In the rat, the percentage of CNP-induced inhibition was 95.87±4.12 %(fundus), 94.91±5.08 % (body) and 66.32±7.32 % (antrum)in the gastric circular smooth muscle, but in the longitudinal smooth muscle, CNP completely inhibited the spontaneous contraction. Using LY83583, a guanylate cyclase inhibitor, and zaparinast as a phosphoesterase inhibitor to inhibit the generation of cGMP, the effect of CNP on the spontaneous contraction was markedly weakened by LY83583, however, the inhibitory effect was enhanced by zaparinast.CONCLUSION: (1) CNP can obviously inhibit the spontaneous contraction of gastric antral circular and longitudinal smooth muscle in the rat, guinea-pig and human.The order of inhibitory potency is human ＞rat＞ guinea-pig.(2) In the same animals, the inhibitory effect of CNP on spontaneous contraction is the most powerful in fundus and the weakest in antrum, in the same position, the inhibitory effect on the circular smooth muscle is more powerful than that on longitudinal smooth muscle. (3) The inhibitory effect of CNP on spontaneous contraction in the gastric smooth muscle is mediated by a cGMP dependent pathway.     

Effects of unsaturated fatty acids on calcium-activated potassium current in gastric myocytes of guinea pigs

AIM: To investigate the effects of exogenous unsaturated fatty acids on calcium-activated potassium current [IK(Ca)] in gastric antral circular myocytes of guinea pigs. METHODS: Gastric myocytes were isolated by collagenase from the antral circular layer of guinea pig stomach. The whole-cell patch clamp technique was used to record /K(Ca) in the isolated single smooth muscle cells with or without different concentrations of arachidonic acid (AA), linoleic acid (LA), and oleic acid (OA). RESULTS: AA at concentrations of 2,5 and 10 μmol/L markedly increased IK(Ca) in a dose-dependent manner. LA at concentrations of 5, 10 and 20 μmol/L also enhanced /K(Ca) in a dose-dependent manner. The increasing potency of AA, LA, and oleic acid (OA) on /K(Ca)at the same concentration (10μmol/L) was in the order of AA>LA>OA. AA (10 μmol/L)-induced increase of Ik(ca) was not blocked by H-7 (10 μmol/L), an inhibitor of protein kinase C (PKC), or indomethacin (10 μmol/L), an inhibitor of the cyclooxygenase pathway, and 17-octadecynoic acid (10 μmol/L), an inhibitor of the cytochrome P450 pathway, but weakened by nordihydroguaiaretic acid (10μmol/L), an inhibitor of the lipoxygenase pathway. CONCLUSION: Unsaturated fatty acids markedly increase Ik(Ca), and the enhancing potencies are related to the number of double bonds in the fatty acid chain. The lipoxygenase pathway of unsaturated fatty acid metabolism is involved in the unsaturated fatty acid-induced increase of IK(Ca) in gastric antral circular myocytes of guinea pigs.     

SD大鼠左心室利钠肽三型受体的表达

目的：研究利钠肽三种亚型受体（NPR—A,NPR—B和NPR—C）是否在正常SD大鼠左心室心肌细胞有表达。方法：应用免疫组织化学和Western免疫印迹检测SD大鼠左室心肌NPR—A、NPR—B和NPR—C的表达。结果：两种方法显示SD大鼠左室心肌有NPR—A、NPR—B和NPR—C三种亚型受体的表达,以NPR—A表达最强,NPR-C表达最弱。结论：正常SD大鼠左室心肌有A、B、C三种利钠肽受体表达。     

Effect of actin microfilament on potassium current in guinea pig gastric myocytes

AIM: To investigate the effect of actin microfilament on potassium current and hyposmotic membrane stretch-induced increase of potassium current in gastric antral circular myocytes of guinea pig. METHODS: Whole-cell patch clamp technique was used to record potassium current in isolated gastric myocyes. RESULTS: When the membrane potential was clamped at -60mV, an actin microfilament disruptor, cytochanlasin-B (Cyt-B, 20μmol/L in pipette) increased calcium-activated potassium current (IK（Ca）) and delayed rectifier potassium current (IK（V）)to 138.4&#177;14.3% and 142.1&#177;13.1%respectively at +60mV. In the same condition, an actin microfilament stabilizer phalloidin (20μmol/L in pipette)inhibited IK（Ca） and IK（V） to 74.2&#177;7.1% and 75.4&#177;9.9% respectively. At the holding potential of -60mV, hyposmotic membrane stretch increased IK（Ca） and IK（V） by 50.6&#177;9.7% and 24.9&#177;3.3% at +60mV respectively. In the presence of cytochalasin-B and phalloidin (20μmol/L, in the pipette)condition, hyposmotic membrane stretch also increased IK（Ca） by 44.5&#177;7.9% and 55.7&#177;9.8% at +60mV respectively. In the same condition, cytochalasin-B and phalloidin also increased IK（V） by 23.0&#177;5.5% and 30.3&#177;4.5% respectively. However, Cyt-B and phalloidin did not affect the amplitude of hyposmotic membrane stretch-induced increase of IK（Ca） and IK（V）. CONCLUSION: Actin microfilaments regulate the activities of potassium channels, but they are not involved in the process of hyposmotic membrane stretch-induced increase of potassium currents in gastric antral circular myocytes of guinea pig.     

四磨汤对大鼠胃窦平滑肌影响及其机制的研究

临床证实四磨汤可改善胃肠动力障碍疾病的症状。但机制不明。目的：研究四磨汤对大鼠离体胃窦平滑肌收缩活动的影响及其机制。方法：处死Sprague-Dawlev大鼠后收集胃窦纵行和环行平滑肌条,检测不同剂量四磨汤（1μl、5μl、25μl、50μl、100μl、150μl和200μl）对胃窦平滑肌收缩的影响,同时观察M受体阻断剂阿托品（100mol／L）、M受体激动剂乙酰胆碱（10-6mol／L）对四磨汤诱导的胃窦平滑肌收缩的影响。结果：低一中剂量（1～100μl）四磨汤剂量依赖性地诱导大鼠胃窦纵行肌和环行肌收缩增强,但两者之间的作用无明显差异。阿托品可完全阻断四磨汤对胃窦环行肌、纵行肌的促收缩作用,且对环行肌的阻断效应更明显。以乙酰胆碱预处理后,四磨汤对胃窦纵行肌和环行肌的促收缩作用进一步增强．且对环行肌的作用更明显。结论：四磨汤对大鼠胃窦纵行肌和环行肌具有明显的促收缩作用．该作用主要通过M受体介导。