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Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第2期34卷 507-514页

作者： Prasad, A Andrews, NP Padder, FA Husain, M Quyyumi, AA NHLBI NIH Cardiol Branch Bethesda MD 20892 USA

OBJECTIVES We investigated whether glutathione (GSH), a reduced thiol that modulates redox state and forms adducts of nitric oxide (NO), improves endothelium-dependent vasomotion and NO activity in atherosclerosis. BACKGROUND Endothelial dysfunction and reduced NO activity are associated with atherosclerosis and its clinical manifestations such as unstable angina. METHODS In the femoral circulation of 17 patients with atherosclerosis or its risk factors, endothelium-dependent vasodilation with acetylcholine (ACH), and endothelium-independent vasodilation with nitroglycerin and sodium nitroprusside were studied before and after GSH. In 10 patients, femoral vein plasma cyclic guanylate monophosphate (cGMP) levels were measured during an infusion of ACH before and after GSH. Femoral artery flow velocity was measured using a Doppler flow wire and the resistance index (FVRI) calculated as mean arterial pressure divided by flow velocity. RESULTS Glutathione strongly potentiated AGH-mediated vasodilation;at the two doses, FVRI decreased by 47% and 56% before, and by 61% and 67% after GSH (p = 0.003). Glutathione also elevated cGMP levels in the femoral vein during ACH infusion from 17.6 +/- 3 to 23.3 rt 3 pmol/ml (p = 0.006). Augmentation of ACH responses was only observed in patients with depressed endothelial function. Glutathione did not influence endothelium-independent vasodilation with either NO donor. CONCLUSIONS Thiol supplementation with GSH selectively improves human endothelial dysfunction by enhancing NO activity. (C) 1999 by the American College of Cardiology.

关键词：乙酰胆碱/药理学动脉硬化/代谢动脉硬化/病理生理学血流速度/药物作用环GMP/血液内皮血管/代谢内皮血管/病理生理学股动脉谷胱甘肽/药理学一氧化氮/代谢一氧化氮供体/药理学硝酸甘油/药理学硝普钠/药理学血管阻力/药物作用血管舒张/药物作用血管舒张/生理学血管舒张药/药理学女(雌)性人类男(雄)性中年人

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4-(3-chloro-4-methoxybenzyl) aminophthalazines: Synthesis and inhibitory activity toward phosphodiesterase 5

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JOURNAL OF MEDICINAL CHEMISTRY 2000年第13期43卷 2523-2529页

作者： Watanabe, N Adachi, H Takase, Y Ozaki, H Matsukura, M Miyazaki, K Ishibashi, K Ishihara, H Kodama, K Nishino, M Kakiki, M Kabasawa, Y Eisai & Co Ltd Tsukuba Res Labs Tsukuba Ibaraki 3002635 Japan

We synthesized various 4-(3-chloro-4-methoxybenzyl)aminophthalazines substituted at the 1- and 6-positions and evaluated their inhibitory activity toward phosphodiesterase 5 (PDE5) and their vasorelaxant activity in isolated porcine coronary arteries precontracted with prostaglandin F2 alpha (10(-5) M). The preferred substituents at the 1-position of the phthalazine were 4-hydroxypiperidino, 4-hydroxymethylpiperidino, 4-(2-hydroxyethyl)piperidino, and 4-oxopiperidino. Among these compounds, [4-(3-chloro-4-methoxybenzyl)amino-1-(4-hydroxy)piperidino]-6-phthalazinecarbonitrile monohydrochloride (13) exhibited potent PDE5 inhibitory activity (IC50 = 0.56 nM) with > 1700-fold high selectivity over other PDE isozymes (PDE1-4). Compound 13 exhibited the most potent vasorelaxant action (EC50 = 13 nM) in this series of compounds. Compound 13 reduced mean pulmonary arterial pressure by 29.9 +/- 3.1% when administered intravenously at 30 mu g/kg to the chronically hypoxic rats and had an apparent oral bioavailability of about 19.5% in rats and was selected for further biological evaluation.

关键词： 3' 5'-环GMP磷酸二酯酶类抗高血压药/化学合成抗高血压药/化学抗高血压药/药代动力学抗高血压药/药理学生物利用度血压/药物作用冠状血管/药物作用冠状血管/生理学环核苷酸磷酸二酯酶类 5型地诺前列素/药理学高血压肺性/药物疗法高血压肺性/病理生理学肌松弛/药物作用肌平滑血管/药物作用肌平滑血管/生理学磷酸二酯酶抑制剂/化学合成磷酸二酯酶抑制剂/化学磷酸二酯酶抑制剂/药代动力学磷酸二酯酶抑制剂/药理学磷酸二酯水解酶类/代谢酞嗪类/化学合成酞嗪类/化学酞嗪类/药代动力学酞嗪类/药理学哌啶类/化学合成哌啶类/化学哌啶类/药代动力学哌啶类/药理学喹唑啉类/药理学大鼠 Sprague-Dawley 构效关系猪血管舒张药/化学合成血管舒张药/化学血管舒张药/药代动力学血管舒张药/药理学动物男(雄)性大鼠

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Synthesis and evaluation of backbone/amide-modified analogs of leualacin

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BIOORGANIC & MEDICINAL CHEMISTRY LETTERS 1999年第4期9卷 563-568页

作者： Hu, MK Yang, FC Chou, CC Yen, MH Natl Def Med Ctr Sch Pharm Taipei 100 Taiwan Natl Def Med Ctr Dept Pharmacol Taipei 100 Taiwan

Leualacin (1), a cyclic depsi-pentapeptide, and its backbone/amide-modified analogs 2-4 were synthesized. Amide analogue 3 exhibited stronger vasodilatory effects. It also strongly inhibited collagen- and arachidonic acid (AA)induced platelet aggregations with IC(50)s of 0.6 mu M and 2.0 mu M, respectively (C) 1999 Elsevier Science Ltd. All rights reserved.

关键词：主动脉/药物作用主动脉/生理学花生四烯酸/药理学胶原/药理学肽类环/化学合成肽类环/化学肽类环/药理学血小板聚集抑制剂/化学合成血小板聚集抑制剂/化学血小板聚集抑制剂/药理学大鼠近交WKY 血栓烷B2/拮抗剂和抑制剂血管舒张药/化学合成血管舒张药/化学血管舒张药/药理学动物大鼠

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Differential sensitivity among nitric oxide donors toward ODQ-mediated inhibition of vascular relaxation

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期292卷 737-742页

作者： Tseng, CML Tabrizi-Fard, MA Fung, HL SUNY Buffalo Sch Pharm Dept Pharmaceut Buffalo NY 14260 USA

Nitric oxide (NO) donors are believed to exert their vasodilatory action through the activation of soluble guanylate cyclase (sGC), the heme site of which can be specifically inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). We examined the vascular relaxation of the rat aorta mediated by eight different NO donors in the presence of ODQ (0.1, 1, or 10 mu M), and demonstrated that these NO donors displayed different sensitivities toward ODQ inhibition (ANOVA, P < .05). Among the NO donors studied, S-nitrosothiols such as S-nitroso-N-acetylpenicillamine (SNAP) and S-nitrosoglutathione exhibited partial resistance toward ODQ inhibition at 0.1 mM ODQ, whereas nitroglycerin (NTG) showed nearly complete inhibition at this concentration of ODQ. Three NO donors representing increasing sensitivity toward ODQ inhibition, SNAP, sodium nitroprusside (SNP), NTG, were chosen for additional mechanistic studies. ODQ (1 mu M) inhibition of vascular relaxation by SNAP and SNP, but not that by NTG, was partially reversed by a sulfhydryl donor, N-acetylpenicillamine (100 mu M), and by a phosphodiesterase inhibitor, zaprinast (10 mu M), specific for cGMP. Our results strongly indicate that the vascular relaxation mechanism(s) of NO donors is not identical for each. In the rat aorta, NTG appeared to exhibit its vasodilatory effect exclusively through activation of the heme site of sGC. On the other hand, in the intact vascular tissue, SNAP and SNP could bring about vasodilation through a secondary pathway. These results are consistent with the view that SNAP and SNP, but not NTG, can induce vascular relaxation additionally through the activation of the sulfhydryl site of sGC.

关键词：主动脉胸剂量效应关系药物药物相互作用鸟苷酸环化酶/拮抗剂和抑制剂一氧化氮供体/药理学硝酸甘油/药理学硝普钠/药理学恶二唑类/药理学青霉胺/类似物和衍生物青霉胺/药理学磷酸二酯酶抑制剂/药理学嘌呤酮类/药理学喹恶啉类/药理学大鼠 Sprague-Dawley 血管舒张药/药理学动物男(雄)性大鼠

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Nocistatin: a novel neuropeptide encoded by the gene for the nociceptin/orphanin FQ precursor

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PEPTIDES 2000年第7期21卷 1101-1109页

作者： Okuda-Ashitaka, E Ito, S Kansai Med Univ Dept Med Chem Moriguchi Osaka 5708506 Japan

We identified a novel neuropeptide and named it "nocistatin." Its presence was expected by analysis of the precursor for the neuropeptide nociceptin or orphanin FQ (Noc/OFQ), previously identified as an endogenous ligand for the orphan opioid receptor-like receptor. The precursor prepronociceptin/orphanin FQ (ppNoc/OFQ) comprises at least two bioactive peptides, nocistatin and Noc/OFQ. Noc/OFQ is involved in a broad range of pharmacological actions in various tissues from the central nervous system to the periphery. In pain transmission, Noc/OFQ is reported to have different effects including nociception, no effect, and analgesia, depending on the animal species tested, doses, route of administration, and so on. We found that intrathecal administration of Noc/OFQ induced pain responses including allodynia and hyperalgesia. Simultaneous administration of nocistatin blocked the allodynia and hyperalgesia induced by Noc/OFQ, whereas anti-nocistatin antibody decreased the threshold for the Noc/OFQ-induced allodynia. The endogenous heptadecapeptide nocistatin was isolated from bovine brains and recently identified in mouse, rat, and human brain and in human cerebrospinal fluid. Although human, rat and mouse ppNoc/OFQ produced larger respective counterparts with 30, 35, and 41 amino acid residues, all peptides showed the antinociceptive activity. This activity was ascribed to the carboxyl-terminal hexapeptide of nocistatin, Glu-Gln-Lys-Gln-Leu-Gln, which is conserved beyond species. Nocistatin also attenuated the allodynia and hyperalgesia evoked by prostaglandin E-2 and the inflammatory hyperalgesia induced by formalin or carrageenan/kaolin, and reversed the Noc/OFQ-induced inhibition of morphine analgesia at picogram doses. Furthermore, nocistatin counteracted the impairment of learning and memory induced by Noc/OFQ or scopolamine. Nocistatin is widely present in the spinal cord and brain. Although nocistatin did not bind to the Noc/OFQ receptor, it bound to the membran

关键词：氨基酸序列镇痛药阿片类/药理学脑/药物作用脑脊髓液/药物作用剂量效应关系药物学习/药物作用记忆/药物作用显微镜检查共焦分子序列数据神经肽类/遗传学神经肽类/药理学阿片样肽类/化学阿片样肽类/遗传学阿片样肽类/药理学阿片样肽类/生理学序列同源性氨基酸时间因素血管舒张药/化学血管舒张药/药理学动物牛人类小鼠大鼠

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Nucleotide modulation of pinacidil stimulation of the cloned K_ATP channel Kir6.2/SUR2A

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MOLECULAR PHARMACOLOGY 2000年第6期57卷 1256-1261页

作者： Gribble, FM Reimann, F Ashfield, R Ashcroft, FM Univ Oxford Physiol Lab Oxford OX1 3PT England

ATP-sensitive K+ channels are the target for K+ channel openers such as pinacidil. These channels are formed from pore-forming Kir6.2 and regulatory sulfonylurea receptor (SUR) subunits. Pinacidil activates channels containing SUR2A (heart, skeletal muscle), but not those containing SUR1 (beta cells). Surprisingly, binding of the pinacidil analog [H-3]P1075 is dependent on added nucleotides, yet in electrophysiological studies, pinacidil is effective in the absence of intracellular nucleotides. To determine the reason for this anomaly, we examined the functional interactions between pinacidil (or P1075) and nucleotides by expressing cloned Kir6.2/SUR2A channels in Xenopus laevis oocytes. Both pinacidil and P1075 activated macroscopic Kir6.2/SUR2A currents in the absence of added nucleotide, but the presence of intracellular ATP or ADP slowed the off-rate of the response. Mutation of the Walker A lysine in a single nucleotide binding domain (NBD) of SUR2A (K707A in NBD1, K1348A in NBD2), abolished this action of nucleotide. The K1348A mutation prevented stimulation by MgADP but had little effect on the amplitude of the pinacidil response. In contrast, Kir6.2/SUR2A-K707A currents were activated by MgADP, but only responded to pinacidil in the presence of Mg-nucleotide. Off-rates in the absence (or presence) of nucleotide were slower for the pinacidil analog P1075 than for pinacidil, consistent with the higher affinity of P1075. We suggest that slowing of P1075 dissociation by nucleotide enables binding to be detected.

关键词：腺苷二磷酸/药理学腺苷三磷酸/药理学抗高血压药/药理学结合部位胍类/药理学突变卵母细胞/代谢吡那地尔/药理学钾通道/化学钾通道/药物作用钾通道/遗传学钾通道/代谢钾通道内向整流蛋白质构象吡啶类/药理学氚血管舒张药/药理学爪蟾光滑动物小鼠

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The effect of ovariectomy and oestrogen replacement on small artery biomechanics in the rat

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BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY 1999年第2期106卷 148-154页

作者： Acs, N Székács, B Nádasy, GL Várbíró, S Kakucs, R Monos, E Semmelweis Univ Med Dept Obstet & Gynaecol 2 H-1082 Budapest Hungary Semmelweis Univ Med Dept Internal Med 2 H-1085 Budapest Hungary Semmelweis Univ Med Clin Res Inst Dept Physiol 2 H-1085 Budapest Hungary

Objective To determine the effects of oestrogen deficiency and hormone replacement therapy on the biomechanical properties of a small artery. Sample Thirty non-pregnant female Sprague-Dawley rats. Methods Twenty animals were pharmacologically ovariectomised by triptorelin and received either oestradiol propionate or its vehicle. Tell other animals received only the vehicle for the same period of time (control group). After 12 weeks of treatment, cylindrical segments of the saphenous artery were isolated and cannulated at both ends. Pressure-diameter curves were recorded from segments in normal Krebs-Ringer, using norepinephrine, and then with papaverine. The vessel segment close to the examined one was histologically evaluated. Serum levels of oestradiol and cortisol were determined. Main outcome measures Biomechanical parameters based on the pressure-diameter curves. Results Pharmacological ovariectomy decreased the passive diameter of the arteries and oestrogen replacement therapy prevented this. Decreased reactivity to norepinephrine was also restored by oestrogen treatment. Pressure induced myogenic tone was decreased significantly by oophorectomy and increased after oestradiol treatment. No significant changes were found in wall thickness, distensibility, elastic modulus or tangential stress. No significant histological alterations were seen in tl le vessel wall. Oestradiol levels were significantly decreased in the castrated animals compared with the other two groups. Conclusions These results suggest that oestrogen deficiency decreases and oestrogen replacement increases the passive diameter of small peripheral arteries, and that oestrogen enhances the reactivity of vascular smooth muscle. These responses may provide the background mechanisms For the increased incidence of arterial hypertension and hot flushes during the menopause and the ability of oestrogen substitution to prevent them.

关键词：动脉/药物作用动脉/病理学动脉/生理学培养技术雌二醇/药理学雌激素替代疗法雌激素类/缺乏雌激素类/生理学黄体溶解剂肌平滑血管/药物作用肌平滑血管/生理学去甲肾上腺素/药理学罂粟碱/药理学大鼠 Sprague-Dawley 双羟萘酸曲普瑞林血管收缩药/药理学血管舒张药/药理学动物女(雌)性大鼠

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An angiogenic switch in macrophages involving synergy between toll-like receptors 2, 4, 7, and 9 and adenosine A_2A receptors

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期163卷 711-721页

作者： Pinhal-Enfield, G Ramanathan, M Hasko, G Vogel, SN Salzman, AL Boons, GJ Leibovich, SJ Univ Med & Dent New Jersey New Jersey Med Sch Dept Cell Biol & Mol Med Newark NJ 07013 USA Univ Med & Dent New Jersey New Jersey Med Sch Dept Surg Newark NJ 07013 USA Univ Maryland Dept Microbiol & Immunol Baltimore MD 21201 USA Inotek Pharmaceut Corp Beverly MA USA Univ Georgia Complex Carbohydrate Res Ctr Athens GA 30602 USA

Adenosine A(2A) receptor (A(2A)R) agonists synergize with Escherichia coli (E. coli) LPS [toll-like receptor (TLR)4 agonist] to up-regulate vascular endothelial growth factor (VEGF) expression in murine macrophages. Here, we demonstrate that TLR2, TLR7. and TLR9, but not TLR3 and TLR5 agonists, also synergize with A(2A)AR agonists and adenosine to up-regulate VEGF, while simultaneously strongly down-regulating TNFalpha expression. in the absence of adenosine or A(2A)R agonists, Porphyromonas gingivalis (P. gingivalis) LPS and PAM(3)CAG (TLR2 agonists), resiquimod (R848) (TLR7 agonist), and non-methylated CpG DNA (TLR9 agonist) strongly up-regulate TNFalpha expression, with no effect on VEGF. In the presence of adenosine or A(2A)R agonists but not A(2A)R agonists, TLR2, 4, 7, and 9 agonists strongly up-regulate VEGF expression, while simultaneously down-regulating TNFalpha. C57BL/ 10ScN (TLR4 deletion mutant) macrophages produce TNFa in response to TLR2, 3, 7, and 9 agonists, but not the TLR4 agonist E. coli LPS. With adenosine or A(2A)R agonists, TLR2, 7, and 9, but not TLR4 agonists, also synergistically up-regulate VEGF, while down-regulating TNFalpha expression. Polyinosinic-polycytidilic acid (poly(I:C)) (TIR3 agonist) stimulates TNFalpha expression in macrophages from both C57BL/10ScSn and C57BL/10ScN mice, but has little effect on VEGF expression in the presence of adenosine or A(2A)R agonists. R-flagellins from Serratia marcescens (S. marcescens) and Salmonella muenchen (S. muenchen) do not stimulate TNFalpha expression in either C57BL/ 10ScSn or C57BL10/ScN mice, and have no effect on VEGF production in the presence of adenosine or A(2A)AR agonists. While adenosine and A(2A)AR agonists strongly down-regulate TNFalpha protein expression induced by TLR2, 3, 4, 7, and 9 agonists, TNFa mRNA and NF-kappaB activation are not reduced. We propose a novel signaling pathway in murine macrophages involving synergy between TLRs 2, 4, 7, and 9 and A(2A)Rs, that up-regula

关键词：腺嘌呤/类似物和衍生物腺嘌呤/药理学腺苷/药理学腺苷-5'-(N-乙基羧基酰胺)/药理学血管生成抑制剂/药理学细胞培养的 DNA结合蛋白质类/激动剂 DNA结合蛋白质类/代谢内皮生长因子/代谢酶抑制剂/药理学胞间信号肽类和蛋白质类/代谢脂多糖类/药理学脂蛋白类/代谢淋巴因子/代谢巨噬细胞腹膜/细胞学巨噬细胞腹膜/药物作用巨噬细胞腹膜/代谢膜糖蛋白类/激动剂膜糖蛋白类/遗传学膜糖蛋白类/代谢小鼠近交C57BL 小鼠基因敲除 NF-κB/代谢新生血管化生理性紫杉酚/药理学受体腺苷A2A 受体细胞表面/激动剂受体细胞表面/遗传学受体细胞表面/代谢受体嘌呤能P1/代谢 Toll样受体2 Toll样受体3 Toll样受体4 Toll样受体5 Toll样受体7 Toll样受体9 Toll样受体肿瘤坏死因子α/遗传学肿瘤坏死因子α/代谢增量调节/生理学血管内皮生长因子A 血管内皮生长因子类血管舒张药/药理学动物人类男(雄)性小鼠

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Sustained infection induces 2 distinct microvascular mechanisms in the splanchnic circulation

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SURGERY 2000年第4期128卷 513-518页

作者： Zhao, HL Spain, DA Matheson, PJ Vaughn, C Harris, PD Garrison, RN Univ Louisville Dept Surg Louisville KY 40292 USA Univ Louisville Dept Physiol & Biophys Louisville KY 40292 USA Univ Louisville Ctr Excellence Appl Microcirculatory Res Louisville KY 40292 USA Vet Affair Med Ctr Louisville KY USA

Background. Altered intestinal bloodflow during systemic inflammation leads to organ dysfunction. Mucosal ischemia occurs during sepsis despite an increase in portal blood flow. We hypothesized that separate mechanisms are active in the large resistance and small mucosal microvessels to account for this dichotomy. Methods. Chronic infection was induced in rats by bacterial inoculation (Escherichia coli and Bacteroides fragilis) of an implanted subcutaneous sponge. Separate groups were studied at 24 and 72 hours after a single inoculation of bacterium or 24 hours after a second inoculation tie, 72 hours of sepsis). Time-matched controls were used for each group. Intravital microscopy of the terminal ileum was used to assess endothelial-dependent vasodilation to acetylcholine (10(-9) to 10(-5) mol/L) resistance (A(1)) and premucosal (A(3)) arterioles. Threshold sensitivity (-log of 20% response dose) was calculated from dose response curves for each animal. Results. Vasodilator sensitivity to acetylcholine in A(1) arterioles was significantly decreased at 24 hours, and these changes persisted up to 72 hours after a single bacterial inoculation. There was no change in the dilator sensitivity of A(3) arterioles after a single inoculation. When. there was a challenge with a second bacterial inoculation, there was a reversal of the A(1) dilator response and an increase in A(3) sensitivity. Conclusions. An initial septic event results in a decrease in dilator reactivity in the resistance A(1) arterioles that;persists for at least 72 hours. A sustained septic challenge results in increased dilator reactivity in both A(1) and A(3) vessels. This enhanced sensitivity during sepsis suggests that more than 1 therapeutic approach to preservation of intestinal bloodflow will be necessary.

关键词：乙酰胆碱/药理学拟杆菌感染/代谢拟杆菌感染/病理生理学拟杆菌脆弱大肠杆菌感染/代谢大肠杆菌感染/病理生理学肠黏膜/血液供给肠黏膜/酶学肠黏膜/病理生理学显微镜检查电视一氧化氮/代谢一氧化氮合酶/代谢大鼠 Sprague-Dawley 脓毒症/代谢脓毒症/病理生理学内脏循环/生理学血管舒张/药物作用血管舒张/生理学血管舒张药/药理学动物男(雄)性大鼠

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Activation of volume-regulated Cl^- channels by ACh and ATP in Xenopus follicles

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第3期525卷 721-734页

作者： Pérez-Samartín, AL Miledi, R Arellano, RO Univ Nacl Autonoma Mexico Ctr Neurobiol Queretaro 76001 Mexico Univ Basque Country Dept Neurociencias Leioa 48940 Vizcaya Spain Univ Calif Irvine Cellular & Mol Neurobiol Lab Irvine CA 92697 USA

1. Osmolarity-dependent ionic currents from follicle-enclosed Xenopus oocytes (follicles) were studied using electrophysiological techniques. Whole follicle currents were monitored using a two-electrode voltage clamp and single-channel activity was measured using the patch-clamp technique. 2. In follicles held at -60 mV two chloride currents were activated in external hyposmotic solutions. One was the habitual volume-regulated current elicited by external hyposmolarity (I-Cl,I-swell), and the second was a slow and smooth current (S-in) generated by BCh or ATP application. 3. In follicles, the permeability ratios for different anions with respect to Cl- were similar for both I-Cl,I-swell and S-in, with a sequence of: SCN- > I- > Br- greater than or equal to NO3- greater than or equal to Cl- > gluconate greater than or equal to cyclamate > acetate > SO42-. 4. Extracellular ATP blocked the outward component of S-in. Also, extracellular pH modulated the inactivation kinetics of S-in elicited by ACh;e.g. inactivation at +80 mV was similar to 100% slower at pH 8.0 compared with that at pH 6.0. 5. Lanthanides inhibited I-Cl,I-swell and S-in. La3+ completely inhibited I-Cl,I-swell with a half-maximal inhibitory concentration (IC50) of 17 +/- 1.9 mu M, while S-in was blocked up to 55% with an apparent IC50 of 38 +/- 2.6 mu M. 6. Patch-clamp recordings in follicular cells showed that hyposmotic challenge opened inward single-channel currents. The single channel conductance (4.7 +/- 0.4 pS) had a linear current-voltage relationship with a reversal membrane potential close to -20 mV. This single-channel activity was increased by application of ACh or ATP. 7. The I-Cl,I-swell generation was not affected by pirenzepine or metoctramine, and did not affect the purinergic activation of the chloride current named F-in. Thus;I-Cl,I-swell was not generated via neurotransmitters released during cellular swelling. 8. All together, equal discrimination for different anions, similar modula

关键词：乙酰胆碱/药理学腺苷三磷酸/药理学阴离子/代谢氯化物通道/生理学氯化物/代谢钆/药理学氢离子浓度低渗溶液/药理学镧/药理学膜电位/药物作用膜电位/生理学金属稀土/药理学神经递质药/代谢卵母细胞/化学卵母细胞/生理学膜片钳术血管舒张药/药理学水电解质平衡/生理学爪蟾光滑动物女(雌)性

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