Mechanisms of pinacidil-induced vasodilatation

The mechanism of the vasodilator effect of pinacidil was examined. Pinacidil (0.1–100 μM) inhibited the increases in cytosolic Ca²⁺ ([Ca²⁺]_i) and muscle tension due to norepinephrine in rat aorta. In contrast, a Ca²⁺ channel blocker, verapamil, inhibited the norepinephrine-stimulated [Ca²⁺]_i more strongly than the contraction. Higher concentrations of pinacidil (3–100 μM) inhibited the verapamil-insensitive portion of the contraction and [Ca²⁺]_i. An inhibitor of ATP-sensitive K⁺ channels, glibenclamide, antagonized the inhibitory effect of low concentrations ( 10 pM) of pinacidol. Pinacidil did not change the contraction induced by Ca²⁺ in vascular smooth muscle permeabilized with Staphylococcus aureus -toxin. Norepinephrine (in the presence of GTP), 12-deoxyphorbol 13-isobutyrate (in the absence of GTP), and treatment with GTP_γS potentiated the contraction of permeabilized smooth muscle induced by the addition of Ca²⁺. Pinacidil (100 μM) inhibited the potentiation due to GTP_γS or noepinephrine but not to phorbol ester. These results suggest that pinacidil has dual effects on vascular smooth muscle contraction. At lower concentrations (>0.1 μM), it decreases [Ca²⁺]_i, possibly by activating ATP-sensitive K+ channels. At higher concentrations (> 3 μM), it may additionally inhibit the receptor-mediated, GTP-binding protein-coupled phosphatidyl inositol turnover.     

推按运经仪为主治疗结石300例

采用推按运经仪加中药、耳穴贴压等综合治疗结石３００例，６０例肝胆结石中，治愈２８例，显效２０例，无效１２例，有效率８０％；２４０例泌尿系结石中，治愈１３６例，显效８８例，无效１６例，有效率９３．３％。     

hNa_v1.8mRNA在三叉神经痛患者痛支神经中的表达

目的：观察河脉毒素不敏感型钠通道Navl．8 mRNA在三叉神经痛(trigeminal neuralgia,TN)患者痛支神经中的表达。方法：利用RT—PCR技术，以β—actin为内参照，检测5例原发性TN保守治疗无效患者的痛支神经、2例行舌颌颈联合根治术患者正常耳大神经和肌肉组织中hNavl．8 mRNA的表达。结泉：hNavl．8 mRNA在TN患者痛支神经中有明显表达，而在正常耳大神经及肌肉组织中均无表达。结论：hNavl．8 mRNA在三叉神经痛支中的异常表达可能与TN的发病机制有关。     

离子通道与弱精子症

弱精子症是引起男性不育的常见病因之一。随着以精子自身为对象的研究深入,发现离子跨膜转运对精子的生理活动起着重要的作用。离子通道病于20世纪90年代提出,现已逐渐发现临床上许多先天性和/或后天获得性疾病与异常的离子通道有关。因此,关于精子的生理和疾病与离子通道的关系研究逐渐成为当前研究的热点之一。现就近年来与精子运动相关的离子通道,包括阳离子通道和阴离子通道的研究进展作一综述。     

玉郎伞提取物对大鼠自发性高血压的影响

目的：研究玉郎伞提取物(YLS)对自发性高血压大鼠(SHR)及正常大鼠血压(BP)的影响。方法：应用颈动脉插管测压法，连接MS2000多媒体生物信号记录系统测定静注YLS前及药后20s、30s、lmin、2min、5min时的收缩压(SP)、舒张压(DP)、平均动脉压(MP)。结果：YLS使SHR及正常大鼠血压明显降低(P＜0．01)，降压作用维持时间较短，给药后5min血压基本恢复正常；YLS对去甲肾上腺素(NA)和异丙肾上腺素（ISO)的作用无明显影响。结论：YLS对正常大鼠及SHR血压有明显的降低作用。     

hCG/ATP-induced Leydig cell calcium channel reaction at different extracellular calcium ion concentration

Objective: To study the calcium channel reaction of human Leydig cells induced by hCG/ATP at different extracellular calcium ion concentrations. Methods: The Leydig cell calcium ion concentration was examined with laser confocal microscope, when the cells were stimulated with hCG/ATP at different extracellular calcium contrations. Results: With calcium-containing extracellular fluid, the Leydig cells were sensitive to hCG stimulation and when the extracellular fluid was calcium-free, the Leydig cells did not respond to the stimulation. However, the Leydig cells did respond to ATP stimulation no matter the extracellular fluid contained calcium or not. Conclusion: In human Leydig cells, there are calcium channels sensitive to hCG and ATP. The extracellular calcium ion concentration plays an important role in the regulation of Leydig cell metabolism by hCG/ATP.     

Modulation of vertebrate neuronal calcium channels by transmitters

A large number of neurotransmitters have now been shown to reduce the amplitude and slow the activation kinetics of whole cell HVA I_Ca in a great diversity of neurons. These transmitters include l-glutamate (AMPA/kainate, metabotropic and NMDA receptors), G AB A (via GABA_B receptors, NA (via α₂ receptors), 5-HT, N A (via α₂ receptors), DA and several peptides. Both whole-cell and single-channel studies have demonstrated that the N-channel is the most common channel type to be blocked by transmitters, although an inhibition of the L-type channel has also occasionally been reported. The suppression of the N-type Ca current was commonly shown to be voltage-dependent, with a relief at large positive voltages. Strong evidence has been put forward showing that the transmitter action is mediated by a G-protein, with GDP-β-S blocking transmitter action, and GTP-γ-S directly inhibiting the Ca channel. Moreover, pertussis toxin blocked the transmitter action in most neurons, and following such block, injection of the G-protein G₀ restored transmitter action. A direct link between the G-protein and the Ca channel has been widely theorized to mediate the action of transmitters on certain neurons. There is also some evidence that certain transmitters in specific neurons mediate calcium channel inhibition through a 2nd messenger, perhaps protein kinase C.Transmitters have also been found, although uncommonly, to inhibit HVA L-type and LVA T-type channels. In addition, an enhancement of both HVA and LVA, Ca currents by transmitters has been demonstrated, and substantial evidence exists for mediation of this action by cAMP.     

Cobalt-dependent potentiation of net inward current density in Helix aspersa neurons.

A low concentration of transition metal ions Co2+ and Ni2+ increases the inward current density in neurons from the land snail Helix aspersa. The currents were measured using a single electrode voltage-clamp/internal perfusion method under conditions in which the external Na+ was replaced by Tris+, the predominant external current carrying cation was Ca2+, and the internal perfusate contained 120 mM Cs+/0 K+; 30 mM tetraethylammonium (TEA) was added externally to block K+ current. In the presence of Co2+ (3 mM) or Ni2+ (0.5 mM) inward Ca2+ currents were stimulated normally by voltage-dependent activation of Ca2+ channels. There was a 5-10% decrease in the rate of rise of the inward current. The principal effect of Co2+ and Ni2+ in increasing the current density seems to be a decrease in the rate at which the inward currents decline during a depolarizing voltage pulse. The results may be due to a decrease in a voltage-dependent or Ca(2+)-dependent outward current and/or an inhibition of Ca2+ channel inactivation. Outward current under these conditions (zero internal K+) was significant and most likely due to Cs+ efflux through the voltage-activated or Ca(2+)-activated nonspecific cation channels. Co2+ is an extremely effective blocker of this outward current. These results are not an artifact of internal perfusion or the special ionic conditions. Intracellular recording of unperfused neurons in normal Helix Ringer's solution showed that the Ca(2+)-dependent action potential duration was increased significantly by low concentrations of Co2+. This result is consistant with the Co(2+)-dependent increase in inward (depolarizing) current seen in voltage-clamp experiments.     

Inward rectifying potassium channels in human malignant glioma cells

Human glioma cells obtained from established cell lines (Tp-276MG, Tp-301MG, Tp-378MG, Tp-483MG and U-251MG) were analyzed for the presence of ion channels with the tight-seal voltage clamp technique. The current-voltage relation revealed a marked inward rectification at hyperpolarizing voltages, due to the presence of inward rectifying K-channels in cells from all studied cell lines. These channels were conducting when the membrane potential was more negative than the K-equilibrium potential. The slope conductance for the inward K-currents (g_Ki) was affected both by [K⁺]_i and [K⁺]₀. g_Ki was proportional to [K⁺]₀ raised to 0.35 or 0.50, of which the larger value was measured in the presence of low [K⁺]_i (25mM). The rectification was not significantly different in cells perfused with Mg-free EDTA-buffered internal solution. Tl⁺ was 3.5 times more permaant than K⁺. g_ki was blocked by Cs⁺ (1 mM) in a voltage-dependent way (more effective in the hyperpolarized membrane), and by Na⁺ (154 mM) depending on voltage and time. From measurements of unitary current events in membrane patches (outside out or cell attached) the conductance of the single inward rectifying channel was estimated to be 27 ± 7 pS. This type of ion channel may be important for K-uptake by glial cells and hence for the K-homeostasis in the brain.     

甲基黄酮醇胺盐酸盐对异丙肾上腺素正性频率作用的影响

本文比较了甲基黄酮醇胺盐酸盐(MFOA)、普萘洛尔(Pro)、维拉帕米(Ver)对异丙肾上腺素(Iso)所致兔离体右心房正性频率作用的影响。Pro使Iso累积浓度反应曲线平行右移,不抑制最大反应,属于典型的竞争性抑制剂,其pA2=8.43;MFOA和Ver使Iso量效曲线向下右移,抑制最大反应,为非竞争性拮抗。MFOA(2×10~(-5)M)和Ver(2×10~(-7)M)分别使最大反应下降19.28％和48.57％,其pD'2值分别为4.07±0.14、6.68±0.15。结果表明MFOA的作用不同于Pro,和Ver相似。