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药物分析杂志 1998年第S1期18卷 199-200页

作者：朱维华俞如英中国药品生物制品检定所 100050

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Activation of soluble guanylyl cyclase by the nitrovasodilator 3-morpholinosydnonimine involves formation of S-nitrosoglutathione

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MOLECULAR PHARMACOLOGY 1998年第1期54卷 207-212页

作者： Schrammel, A Pfeiffer, S Schmidt, K Koesling, D Mayer, B Graz Univ Inst Pharmakol & Toxikol A-8010 Graz Austria Free Univ Berlin Inst Pharmakol D-14195 Berlin Germany

Soluble guanylyl cyclase (sGC) is the major physiological target of sydnonimine-based vasodilators such as molsidomine. Decomposition of sydnonimines results in the stoichiometric formation of nitric oxide (NO) and superoxide (O-2(radical anion)) which rapidly react to form peroxynitrite. Inasmuch as sGC is activated by NO but not by peroxynitrite, we investigated the mechanisms underlying sGC activation by 3-morpholinosydnonimine (SIN-1). Stimulation of purified bovine lung sGC by SIN-1 was found to be strongly dependent on glutathione (GSH). By contrast, GSH did not affect sGC activation by NO released from 2,2-diethyl-1-nitroso-oxyhydrazine, indicating that NO/O-2(radical anion) released from SIN-1 converted GSH to an activator of sGC. High performance liquid chromatography identified this product as the thionitrite S-nitrosoglutathione. Further, the reaction product decomposed to release NO upon addition of Cu(NO3)(2) in the presence of GSH. Activation of sGC was antagonized by the Cu(I)-specific chelator neocuproine, whereas the Cu(II)-selective drug cuprizone was less potent. Carbon dioxide (delivered as NaHCO3) antagonized S-nitrosation by peroxynitrite but not by SIN-1. Thus, NO/O-2(radical anion) released from SIN-1 mediates a CO2-insensitive conversion of GSH to S-nitrosoglutathione, a thionitrite that activates sGC via trace metal-catalyzed release of NO. These results may provide novel insights into the molecular mechanism underlying the nitrovasodilator action of SIN-1.

关键词： Glutathione Guanylate Cyclase Molsidomine Nitroso Compounds Vasodilator Agents 谷胱甘肽鸟苷酰环化酶吗多明亚硝基化合物血管舒张药 3-morpholino-sydnonimine Glutathione Peroxynitrite nitroso compounds Molsidomine Guanylate Cyclase NOBELIUM Vasodilator Agents Soluble Guanylate Cyclase S-Nitrosoglutathione

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Clinical pharmacokinetics of vasodilators - Part I

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CLINICAL PHARMACOKINETICS 1998年第6期34卷 457-482页

作者： Kirsten, R Nelson, K Kirsten, D Heintz, B Goethe Univ Frankfurt Dept Clin Pharmacol D-60590 Frankfurt Germany Univ Jena Dept Internal Med Jena Germany Rhein Westfal TH Aachen Dept Internal Med 2 Aachen Germany

Understanding the mechanism of action and the pharmacokinetic properties of vasodilatory drugs facilitates optimal use in clinical practice. It should be kept in mind that a drug belongs to a class but is a distinct entity, sometimes derived from a prototype to achieve a specific effect. The most common pharmacokinetic drug improvement is the development of a drug with a half-life sufficiently long to allow an adequate once-daily dosage, Developing a controlled release preparation can increase the apparent half-life of a drug. Altering the molecular structure may also increase the half-life of a prototype drug. Another desirable improvement is increasing the specificity of a drug, which may result in fewer adverse effects, or more efficacy at the target site. This is especially important for vasodilatory drugs which may be administered over decades for the treatment of hypertension, which usually does not interfere with subjective well-being. Compliance is greatly increased with once-daily dosing. Vasodilatory agents cause relaxation by either a decrease in cytoplasmic calcium, an increase in nitric oxide (NO) or by inhibiting myosin light chain kinase. They are divided into 9 classes: calcium antagonists, potassium channel openers, ACE inhibitors, aneiotensin-II receptor antagonists, alpha-adrenergic and imidazole receptor antagonists, beta(1)-adrenergic agonists, phosphodiesterase inhibitors, eicosanoids and NO donors. Despite chemical differences, the pharmacokinetic properties of calcium antagonists are similar. Absorption from the gastrointestinal tract is high, with all substances undergoing considerable first-pass metabolism by the liver, resulting in low bioavailability and pronounced individual variation in pharmacokinetics. Renal impairment has little effect on pharmacokinetics since renal elimination of these agents is minimal. Except for the newer drugs of the dihydropyridine type, amlodipine, felodipine, isradipine, nilvadipine, nisoldipine and nitrendi

关键词： Vasodilator Agents Angiotensin-Converting Enzyme Inhibitors Antihypertensive Agents 血管舒张药 Pharmaceutical Preparations Calcium Channel Blockers Antihypertensive Agents Vasodilator Agents Half Life Angiotensin-Converting Enzyme Inhibitors Myosin-Light-Chain Kinase

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Sodium nitroprusside enhances contractions of the guinea-pig isolated vas deferens

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JOURNAL OF PHARMACY AND PHARMACOLOGY 1998年第2期50卷 205-209页

作者： Ventura, S Hoyle, CHV Burnstock, G Univ London Univ Coll Dept Anat & Dev Biol London WC1E 6BT England

The effects of sodium nitroprusside on the electrical and mechanical properties of the smooth muscle of the guinea-pig vas deferens, and its responses to transmitter substances, have been investigated by use of the sucrose-gap technique. Isolated longitudinal segments of guinea-pig vas deferens contracted in response to electrical field stimulation (100 V, 0.04-0.1 ms, 1-5 Hz, 10 s train every 60 s) and application of ATP (1 mM) or noradrenaline (10 mu M). Sodium nitroprusside (0.1 mM) did not affect resting tension but did enhance contractions evoked by electric-field stimulation but not by ATP or noradrenaline. The sodium nitroprusside-induced enhancement was unaffected by the nitric oxide synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME) (0.1 mM). Conversely, electrically evoked contractions were unaffected by the nitric oxide precursor L-arginine (1 mM) or the nitric oxide donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) (0.1 mM). The amplitudes of electrically evoked excitatory junction potentials (EJPs) were not affected by application of sodium nitroprusside, although it caused a small depolarization of 0.7 +/- 0.3 mV. Similarly, the depolarization caused by exogenous application of ATP or noradrenaline was unaffected by the presence of sodium nitroprusside. L-NAME, L-arginine and SNAP did not affect EJP amplitude or baseline membrane potential. It is concluded that sodium nitroprusside enhances electrically evoked contractions of the guinea-pig vas deferens by reducing the threshold voltage for action potential firing in smooth-muscle cells.

关键词： Antihypertensive Agents Muscle Contraction Muscle Smooth Nitroprusside 抗高血压药肌收缩肌平滑硝普钠输精管血管舒张药 Nuclear auxiliary power systems muscles Nitroprusside Contractions Vas Deferens Norepinephrine Sodium Nitroprusside Antihypertensive Agents Muscle Contraction Electricity Adenosine Triphosphate Guinea Pig threshold voltage

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环氧二羟基前列腺二烯酸长期治疗可降低原发性肺性高血压的肺血管阻力

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中华医学信息导报 1998年第11期13卷 19-20页

作者：杨晓光

据《The New England Journal of Medicine》1998年338卷第5期报道原发性(自发性)肺性高血压用抗凝剂和血管舒张药常规治疗可改善选择性病例的症状和存活期,但没有证据说明该病可以逆转。美国芝加哥拉什医学院及其它医学中心的一组研... 详细信息

据《The New England Journal of Medicine》1998年338卷第5期报道原发性(自发性)肺性高血压用抗凝剂和血管舒张药常规治疗可改善选择性病例的症状和存活期,但没有证据说明该病可以逆转。美国芝加哥拉什医学院及其它医学中心的一组研究人员,对长期(即一年以上)

关键词：肺性高血压前列腺原发性二烯酸长期治疗总肺血管阻力血管舒张药二羟基环氧改善选择性

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Buflomedil is a potent interfering substance in immunoassays of tricyclic antidepressants

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JOURNAL OF ANALYTICAL TOXICOLOGY 1998年第3期22卷 254-254页

作者： Mura, P Kintz, P Robert, R Papet, Y CHU Toxicol Lab F-86021 Poitiers France Inst Med Legale F-67000 Strasbourg France

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酰氨基吲哚衍生物的制备方法

酰氨基吲哚衍生物的制备方法

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作者： J·E·梅卡美国纽约州

式Ⅰ化合物及其药学上可接受的盐，式中R1、R2、R6、n、m、W及Y的定义见说明书。它们可用于治疗偏头痛和其它疾病以及用于精神疗法并且是有效的5-羟色胺(5-HT1)激动剂，可用于治疗抑郁、焦虑、由饮食所致疾病、肥胖、药物滥用、集聚性... 详细信息

标准号: CN1038506C

式Ⅰ化合物及其药学上可接受的盐，式中R₁、R₂、R₆、n、m、W及Y的定义见说明书。它们可用于治疗偏头痛和其它疾病以及用于精神疗法并且是有效的5-羟色胺(5-HT₁)激动剂，可用于治疗抑郁、焦虑、由饮食所致疾病、肥胖、药物滥用、集聚性头痛、偏头痛、疼痛和慢性阵发性偏头痛以及与血管性疾病有关的头痛和由血清作用的神经递质缺乏所致的其它疾病；也可用作中枢性抗高血压和血管舒张药。

关键词：头痛疾病化合物及其药学慢性阵发性偏血管舒张药血管性疾病治疗偏头痛精神疗法神经递质血清作用药物滥用治疗抑郁激动剂偏头痛中枢性羟色胺肥胖高血压焦虑疼痛饮食

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minoxidil/must-see/NAAQS等

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当代外语研究 1998年第7期 24-24页

作者：张福基

长压定,敏乐定(分子式C9H15N5O;周围血管舒张药,口服用于治疗高血压;时下为大家所关注的是,将其溶于丙二醇溶液中能促进一些类型秃发的头发重新生长)

长压定,敏乐定(分子式C₉H₁₅N₅O;周围血管舒张药,口服用于治疗高血压;时下为大家所关注的是,将其溶于丙二醇溶液中能促进一些类型秃发的头发重新生长)

关键词：血管舒张药敏乐定丙二醇长压定分子式头发高血压汽油支原体轮胎

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用于心绞痛和动脉硬化的冠状血管舒张药

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现代药物与临床 1995年第4期10卷 185-186页

作者：冰华

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一种制备苯并杂环化合物或其盐的方法

一种制备苯并杂环化合物或其盐的方法

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作者：小川英则近藤一见山下博司中矢贤治小松一田中理纪北野和良富永道明薮内洋一日本东京

下式新的苯并杂环化合物或其盐;其中R1是H，卤素，OH，等；R2是H，烷基，卤素或烷氧基；R3是苯基链烷酰氨基，或;R4是H，-NR6R7，链烯氧基，HO-烷基，-O-CO-A-NR8R9，等；R5是H，OH，等。该化合物具有优良的加压素拮抗活性，可用作血管... 详细信息

标准号: CN1035670C

下式新的苯并杂环化合物或其盐;其中R¹是H，卤素，OH，等；R²是H，烷基，卤素或烷氧基；R³是苯基链烷酰氨基，或;R⁴是H，-NR⁶R⁷，链烯氧基，HO-烷基，-O-CO-A-NR⁸R⁹，等；R⁵是H，OH，等。该化合物具有优良的加压素拮抗活性，可用作血管舒张药，低血压药，水利尿药，血小板凝集抑挤剂，及含有该化合物作为活性组分的加压素拮抗组合物。

关键词：加压素化合物低血压血管舒张药血小板凝集杂环化合物活性组分烷氧基组合物链烷尿药水利

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