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浙江大学学报（医学版） 2006年第1期35卷 29-33页

作者：周新妹姚慧夏满莉曹春梅蒋惠娣夏强嘉兴学院医学院生理学教研室浙江嘉兴314000 浙江大学医学院生理学教研室浙江杭州310031 浙江大学药学院浙江杭州310031

目的:比较研究槲皮素与芦丁对离体大鼠胸主动脉环的作用及其可能的途径。方法:采用累积加药法,检测槲皮素和芦丁对去氧肾上腺素(pheny lephrine,PE)预收缩的胸主动脉环张力的影响。结果:槲皮素对离体大鼠内皮完整和去内皮的胸主动脉环... 详细信息

目的:比较研究槲皮素与芦丁对离体大鼠胸主动脉环的作用及其可能的途径。方法:采用累积加药法,检测槲皮素和芦丁对去氧肾上腺素(pheny lephrine,PE)预收缩的胸主动脉环张力的影响。结果:槲皮素对离体大鼠内皮完整和去内皮的胸主动脉环均有浓度依赖性的舒张作用,而芦丁对PE预收缩血管的舒张作用是内皮依赖性的。槲皮素和芦丁对内皮完整的胸主动脉环的最大舒张反应分别为(77.20±6.11)%和(44.28±7.48)%,但两者对内皮完整的胸主动脉环最大舒张的半数有效浓度无明显差异。用一氧化氮合酶抑制剂L-NAM E(0.1 mm o l/L)预处理后,可阻断芦丁诱导的舒张血管作用,但不能阻断槲皮素引起的舒张血管作用;用鸟苷酸环化酶抑制剂亚甲蓝(10μm o l/L)预处理后,两者的血管舒张作用均被阻断。用环氧合酶抑制剂吲哚美辛(10μm o l/L)预处理后可减弱槲皮素诱导的舒张血管作用,但不能阻断芦丁引起的舒张血管作用。结论:槲皮素的舒血管作用强于芦丁,槲皮素可能是通过鸟苷酸环化酶和环氧合酶途径产生非内皮依赖性的血管舒张作用,而芦丁可能是通过NO-鸟苷酸环化酶途径产生内皮依赖性的血管舒张作用。

关键词：血管舒张药/药理学槲皮素/药理学芦丁/药理学主动脉,胸/药物作用内皮,血管

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黄芪舒张血管平滑肌的作用及机制

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浙江大学学报（医学版） 2005年第1期34卷 65-68,72页

作者：张必祺胡申江单绮娴孙坚夏强浙江大学医学院附属第一医院浙江杭州310003 浙江大学医学院生理学教研室浙江杭州310031

目的 :探讨黄芪对血管平滑肌的舒张作用及其机制。方法 :采用大鼠离体胸主动脉环灌流模型。在去除血管环内皮后 ,观察累积浓度黄芪对基础状态 (基础组 )、苯肾上腺素 (PE)预收缩 (苯肾上腺素组 )、氯化钾预收缩(氯化钾组 )的血管环的作... 详细信息

目的 :探讨黄芪对血管平滑肌的舒张作用及其机制。方法 :采用大鼠离体胸主动脉环灌流模型。在去除血管环内皮后 ,观察累积浓度黄芪对基础状态 (基础组 )、苯肾上腺素 (PE)预收缩 (苯肾上腺素组 )、氯化钾预收缩(氯化钾组 )的血管环的作用和黄芪对经无钙液 (无钙液组 )、无钙液加肝素 (肝素组 )、普萘洛尔 (普萘洛尔组 )预处理后的血管环的作用。结果 :在血管内皮被去除后 ,黄芪对基础状态或氯化钾预收缩的血管环无影响 ;当黄芪浓度累积达 (10 -1、3× 10 -1、10 0 、3× 10 0 ) g/L时 ,对 PE(3× 10 -7mol/L)预收缩的血管环产生剂量依赖性舒张作用 (P<0 .0 5 )。经无钙液预处理后 ,黄芪 (3× 10 0 g/L )对血管环的舒张作用未被阻断 ;但经无钙液加肝素预处理后 ,该作用被显著抑制 (P<0 .0 1) ;而普萘洛尔预处理不影响黄芪对 PE预收缩血管环的舒张作用。结论 :黄芪对去除内皮的血管具有舒张作用。其机制可能与阻断血管平滑肌细胞内质网上的三磷酸肌醇敏感的钙离子通道 ,抑制内钙的释放有关。

关键词：黄芪/药理学血管舒张药/药理学胸主动脉环/药物作用磷酸肌醇类

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Inhaled nitric oxide attenuates increased pulmonary artery pressure following diaspirin crosslinked hemoglobin (DCLHb) administration

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ARTIFICIAL CELLS BLOOD SUBSTITUTES AND IMMOBILIZATION BIOTECHNOLOGY 1999年第3期27卷 203-213页

作者： Sefton, W Pudimat, P Bina, S Lojeski, E Mongan, P Muldoon, S Uniformed Serv Univ Hlth Sci Dept Anesthesiol Bethesda MD 20814 USA

Intravenous administration of diaspirin crosslinked hemoglobin (DCLHb) can result in elevated pulmonary and systemic arterial pressures in some mammalian species. This study was designed to evaluate the ability of inhaled nitric oxide (INO) to attenuate elevations in pulmonary artery pressure in a closed-chested swine model. Yorkshire pigs received escalating doses of INO followed by escalating doses of DCLHb or a single dose of DCLHb followed by escalating doses of INO. Systemic and pulmonary arterial pressures were monitored continuously. Significant elevations occurred in systemic and pulmonary arterial pressure following a cumulative dose of 0.1 gm/kg DCLHb. A single dose of 0.3 gm/kg also resulted in elevations of pulmonary and systemic arterial pressure. Inhaled nitric oxide partially reversed the changes in pulmonary but not systemic pressure. These results indicate that INO might be a therapeutic option for humans who may experience increased pulmonary artery pressure following administration of DCLHb.

关键词：投药吸入阿司匹林/类似物和衍生物阿司匹林/药理学血气分析血压/药物作用血液代用品/药理学血红蛋白类/药理学高铁血红蛋白血症/血液一氧化氮/药理学肺动脉/药物作用肺动脉/生理学猪血管舒张药/药理学动物女(雌)性男(雄)性

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The insertion/deletion polymorphism of the angiotensin-converting enzyme gene determines coronary vascular tone and nitric oxide activity

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第5期36卷 1579-1586页

作者： Prasad, A Narayanan, S Waclawiw, MA Epstein, N Quyyumi, AA NHLBI NIH Cardiol Branch Bethesda MD 20892 USA

OBJECTIVES We investigated whether the insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene modulates vasomotor tone and endothelial function. BACKGROUND The deletion allele of the ACE I/D polymorphism has been associated with increased incidence of cardiovascular pathology. The risk is synergistically increased in patients who also possess the C allele at position 1,166 of the angiotensin type I (AT1) receptor gene. METHODS In 177 patients with coronary atherosclerosis or its risk factors, we investigated endothelial function with intracoronary acetylcholine (ACH), endothelium-independent smooth muscle function with sodium nitroprusside (SNP) and basal nitric oxide activity with L-N-G monomethyl arginine. RESULTS Compared with ACE II genotype, patients with the ACE DD genotype had lower coronary microvascular and epicardial responses with SNP (coronary blood flow increase 196 +/- 26% vs. 121 +/- 11%, p = 0.003, and diameter increase 21.9 +/- 2% vs. 17 +/- 1%, p = 0.03, ACE II vs. DD, respectively). L-N-G monomethyl arginine induced greater constriction in patients with the ACE DD compared with ACE II genotype (coronary blood flow -10 +/- 4% vs. 11 +/- 5%, p = 0.003, ACE DD vs. II and diameter constriction -6.3 +/- 1.2% vs. -1.9 +/- 1.2%, p = 0.01, respectively, in patients with atherosclerosis). No difference in ACH mediated vasomotion was detected between the three ACE genotypes. The AT1 receptor polymorphism did not influence responses to tither SNP or ACH. CONCLUSIONS Patients possessing the D allele of the ACE gene have increased vascular smooth muscle tone. The enhanced tone appears tu be counterbalanced by an increase in basal nitric oxide activity in patients with atherosclerosis. (C) 2000 by the American College of Cardiology.

关键词：乙酰胆碱/药理学冠状动脉疾病/遗传学冠状动脉疾病/病理生理学冠状血管/药物作用冠状血管/病理生理学基因缺失基因型肌张力/药物作用肌张力/遗传学肌张力/生理学肌平滑血管/药物作用肌平滑血管/病理生理学一氧化氮/生理学硝普钠/药理学肽基二肽酶A/遗传学多态现象遗传血管舒张药/药理学 ωN-甲基精氨酸/药理学人类中年人

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A high-fat diet induces and red wine counteracts endothelial dysfunction in human volunteers

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LIPIDS 2000年第2期35卷 143-148页

作者： Cuevas, AM Guasch, V Castillo, O Irribarra, V Mizon, C San Martin, A Strobel, P Perez, D Germain, AM Leighton, F Pontificia Univ Catolica Chile Sch Med Dept Nutr Santiago Chile Pontificia Univ Catolica Chile Sch Med Dept Metab & Diabet Santiago Chile Pontificia Univ Catolica Chile Sch Med Dept Obstet & Gynecol Santiago Chile Pontificia Univ Catolica Chile Fac Biol Sci Biochem Cytol & Lipids Lab Santiago Chile

Endothelial dysfunction is associated with atherogenesis and oxidative stress in humans. In rat and rabbit blood vessels, wine polyphenol antioxidants induce vascular relaxation in vitro through the NO-cCMP pathway. To assess the effect of a regular high-fat diet (HFD) and moderate red wine consumption on endothelial function (EF), a study was performed in healthy male volunteers. EF was measured as flow-mediated dilatation of the brachial artery, employing high-resolution ultrasound after an overnight fast. Other clinical and biochemical parameters related to EF were also measured. Six volunteers received a control diet, rich in fruits and vegetables (27% calories as fat) and five volunteers received an HFD (39.5% calories as fat). Measurements were done twice on each volunteer: after a period of 30 d with diet plus 240 mt of red wine/d, and after a period of 30 d with diet, without wine. In the absence of wine, there is a reduction of EF with HFD when compared to the control diet (P = 0.014). This loss of EF is not seen when both diets are supplemented with wine for 30 d (P = 0.001). Plasma levels of n-3 fatty acids (R-2 = 0.232, P = 0.023) and lycopene (R-2 = 0.223, P = 0.020) show a positive correlation with individual EF measurements, but they do not account for the significant differences observed among dietary groups or after wine supplementation. These results help elucidate the deleterious effect of a high-fat diet and the protective role of wine, n-3 fatty acids and dietary antioxidants in cardiovascular disease.

关键词：碱性磷酸酶/血液肱动脉/药物作用肱动脉/生理学膳食膳食脂肪类/副作用内皮血管/药物作用内皮血管/生理学脂肪酸类/血液脂肪酸类 ω3/血液水果高半胱氨酸/血液硝酸甘油/药理学转氨酶类/血液血管舒张/药物作用血管舒张药/药理学蔬菜维生素B12/血液葡萄酒 γ-谷氨酰转移酶/血液人类男(雄)性

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β-Adrenergic relaxation of rabbit tracheal smooth muscle:: A receptor deficit that improves with corticosteroid administration

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期292卷 280-287页

作者： Schramm, CM Univ Connecticut Sch Med Pediat Pulm Div Farmington CT USA Childrens Hosp Philadelphia Philadelphia PA USA Univ Penn Sch Med Philadelphia PA 19104 USA

beta-Adrenergic agonists are potent relaxing agents of airway smooth muscle;however, they are often incapable of fully reversing agonist-mediated contractions. The present study was designed to quantitate the relationship between beta-adrenoceptor binding, signal transduction, and relaxation in rabbit tracheal smooth muscle (TSM). TSM segments contracted with acetylcholine to 25 to 75% maximal contraction were relaxed with cumulative administration of isoproterenol (ISO). A beta-adrenergic receptor "deficit" was found, such that incomplete relaxation was achieved with full receptor occupancy. Binding studies with [H-3] dihydroalprenolol demonstrated a beta-adrenoceptor density of 33.1 +/- 8.6 fmol/mg protein in control TSM. Paired studies were performed in TSM from rabbits treated with dexamethasone. Relative to control tissues, dexamethasone-treated TSM displayed twice as much relaxation and cAMP production in response to ISO and twice the beta-adrenoceptor density (82.2 +/- 12.3 fmol/mg protein). Dexamethasone did not affect Gi function, as assessed by the degree of functional antagonism exerted by acetylcholine on ISO-induced relaxations, or beta-adrenoceptor-G(s) coupling, as reflected in high-affinity beta-agonist binding. Collectively, these results demonstrate that corticosteroid administration exerts parallel potentiating effects on beta-adrenoceptor expression and function in rabbit airway smooth muscle.

关键词：乙酰胆碱/药理学肾上腺皮质激素类/药理学肾上腺素能β激动剂/药理学消炎药/药理学环AMP/代谢地塞米松/药理学二氢烯丙洛尔/代谢剂量效应关系药物药物相互作用 GTP结合蛋白质α亚单位 Gi-Go/生理学异丙肾上腺素/药理学肌松弛/药物作用肌平滑/药物作用蛋白质结合放射配体测定受体肾上腺素能β/代谢气管/药物作用血管舒张药/药理学动物兔

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Improvement of peripheral endothelial dysfunction by acute vitamin C application:: Different effects in patients with coronary artery disease, ischemic, and dilated cardiomyopathy

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AMERICAN HEART JOURNAL 2003年第2期146卷 280-285页

作者： Erbs, S Gielen, S Linke, A Möbius-Winkler, S Adams, V Baither, Y Schuler, G Hambrecht, R Univ Leipzig Herzzentrum Dept Internal Med & Cardiol D-04289 Leipzig Germany

Background Endothelial dysfunction has been described in patients with coronary artery disease (CAD) or chronic heart failure (CHF). Vitamin C administration leads to an improvement of endothelial function by reducing elevated levels of reactive oxygen species. It remains unclear, however, whether the degree of endothelial dysfunction caused by oxidative stress differs between CAD and CHF because of ischemic (ICM) or dilated cardiomyopathy (DCM). Methods In patients with CAD (n = 9;left ventricular ejection fraction [LVEF], 64% +/- 3%), ICM (n = 9;LVEF, 25% 4%), DCM (n = 9;LVEF, 25% +/- 3%), and healthy subjects (HS;n = 5;LVEF, 66% +/- 5%) a change in internal radial artery diameter in response to acetylcholine (Ach;15 and 30 mug/min) was measured with high-resolution ultrasound scanning during a co-infusion of normal saline or vitamin C (25 mg/min). Results Ach-mediated vasodilation was blunted in patients with CHF (DCM, 90 +/- 20 mum;ICM, 86 +/- 20 mum) and patients with CAD (336 +/- 20 mum) as compared with HS (496 +/- 43 mum;P <.05 vs patients with DCM, ICM, CAD). Vitamin C co-infusion increased Ach-mediated-vasodilation by 180 +/- 35 mu m (to 270 +/- 30 mu m) in DCM (P <.05 vs CAD, HS) and by 294 +/- 40 mum (to 380 +/- 20 mum) in ICM (P <.05 vs DCM, CAD, HS). In patients with CAD, vitamin C increased Ach-mediated vasodilation by 146 +/- 35 mu m to normal values, whereas vascular diameter remained unchanged in HS (14 +/- 20 mu m;P = not significant) Conclusions Acute vitamin C administration restored peripheral endothelial function in patients with CAD to normal values, whereas endothelial function remained attenuated in CHF, in particular in patients with DCM. These results suggest that in patients with. CHF, factors other than oxidative stress (eg, cytokines) contribute to the pathologic endothelial function.

关键词：心肌缺血/并发症硝普钠/药理学氧化性应激/药物作用血管舒张/药物作用血管舒张药/药理学人类男(雄)性中年人

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期291卷 308-313页

作者： Inoue, M Shimohira, I Yoshida, A Zimmer, A Takeshima, H Sakurada, T Ueda, H Nagasaki Univ Sch Pharmaceut Sci Dept Mol Pharmacol & Neurosci Nagasaki 8528521 Japan NIMH Genet Sect Bethesda MD 20892 USA Univ Tokyo Fac Med Dept Pharmacol Tokyo 113 Japan Daiichi Coll Pharmaceut Sci Dept Biochem Fukuoka 815 Japan

We previously reported that the intraplantar (***.) application of nociceptin/orphanin FQ (N/OFQ) at extremely low doses elicited a nociception through a substance P (SP) release from nociceptor endings. In the present study, the nociception induced by SP (and N/OFQ) was abolished by intrathecal (i.t.) injection of neurokinin(1) (SP receptor) antagonist, suggesting the involvement of the stimulation of nociceptive primary SP neuron and SP release into spinal synapses. On the other hand, similar low doses of N/OFQ (i.t.) exerted nociceptive responses, characterized by scratching, biting, and licking, and these responses were blocked by an neurokinin(1) antagonist (i.t.) or capsaicin pretreatment or in tachykinin 1 gene knockout mice (tac1(-/-) mice), suggesting that N/OFQ receptor (NOR) also exists on the spinal terminals of SP neurons. When wide ranges of N/OFQ doses were used, a typical bell-shaped dose-response relationship was observed in both peripheral and central nociception tests. Furthermore, N/OFQ (1 nmol) administered ***. blocked SP (***.)-induced flexor responses, which were abolished by pertussis toxin pretreatment or in NOR gene knockout (NOR-/-) mice. On the other hand, N/OFQ administered i.t. blocked SP (i.t.)-induced scratching, biting, and licking in capsaicin-pretreated and tac1(-/-) mice, and this antinociception was abolished in NOR-/- mice. All these findings suggest that N/OFQ has biphasic actions depending on doses in the nociceptors and spinal synapses and has postsynaptic antinociceptive actions in spinal cord by modulating SP signaling.

关键词：镇痛药/药理学剂量效应关系药物药物相互作用神经元/药物作用神经元/代谢疼痛感受器/药物作用疼痛感受器/代谢阿片样肽类/药理学疼痛测定脊髓/药物作用脊髓/代谢 P物质/代谢突触/药物作用突触/代谢血管舒张药/药理学动物男(雄)性小鼠

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Nitric oxide inhibits L-type Ca²⁺ current in glomus cells of the rabbit carotid body via a cGMP-independent mechanism

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JOURNAL OF NEUROPHYSIOLOGY 1999年第4期81卷 1449-1457页

作者： Summers, BA Overholt, JL Prabhakar, NR Case Western Reserve Univ Sch Med Dept Phys & Biophys Cleveland OH 44106 USA

Previous studies have shown that nitric oxide (NO) inhibits carotid body sensory activity. To begin to understand the cellular mechanisms associated with the actions of NO in the carotid body, we monitored the effects of NO donors on the macroscopic Ca(2+) current in glomus cells isolated from rabbit carotid bodies. Experiments were performed on freshly dissociated glomus cells from adult rabbit carotid bodies using the whole cell configuration of the patch-clamp technique. The NO donors sodium nitroprusside (SNP;600 mu M, n = 7) and spermine nitric oxide (SNO;100 mu M, n = 7) inhibited the Ca(2+) current in glomus cells in a voltage independent manner. These effects of NO donors were rapid in onset and peaked within 1 or 2 min. In contrast, the outward K(+) current was unaffected by SNP (600 mu M, n = 6), indicating that the inhibition by SNP was not a nonspecific membrane effect. 2-(4-carboxyphenyl)-4, 4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy-PTIO;500 mu M). an NO scavenger, prevented inhibition of the Ca(2+) current by SNP (n = 7), whereas neither superoxide dismutase (SOD;2,000 U/ml, n = 4), a superoxide scavenger, nor sodium hydrosulfite (SHS;1 mM, n = 7), a reducing agent, prevented inhibition of the Ca(2+) current by SNP. However, SNP inhibition of the Ca(2+) current was reversible in the presence of either SOD or SHS. These results suggest that NO itself inhibits Ca(2+) current in a reversible manner and that subsequent formation of peroxynitrites results in irreversible inhibition. SNP inhibition of the Ca(2+) current was not affected by 30 mu M LY 83,583 (n = 7) nor was it mimicked by 600 mu M 8-bromoguanosine 3':5'-cyclic monophosphate (8-Br-cGMP;n = 6), suggesting that the effects of NO on the Ca(2+) current are mediated, in part, via a cGMP-independent mechanism. N-ethylmaleimide (NEM;2.5 mM, n = 6) prevented the inhibition of the Ca(2+) current by SNP, indicating that SNP is acting via a modification of sulfhydryl groups on Ca(2+) channel

关键词：氨基喹啉类/药理学钙/代谢钙通道/生理学钙通道 L型颈动脉体/化学颈动脉体/细胞学颈动脉体/药物作用细胞培养的氰化物/药理学环GMP/类似物和衍生物环GMP/代谢环GMP/药理学连二亚硫酸盐/药理学电生理学酶抑制剂/药理学乙基马来酰亚胺/药理学离子通道闸门/药物作用离子通道闸门/生理学膜电位/药物作用膜电位/生理学一氧化氮/药理学亚硝酸盐类/代谢硝普钠/药理学钾/代谢钾通道/生理学超氧化物歧化酶/药理学血管舒张药/药理学动物兔

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Inositol phosphate metabolism and nitric-oxide synthase activity in endothelial cells are involved in the vasorelaxant activity of nebivolol

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期292卷 698-703页

作者： Parenti, A Filippi, S Amerini, S Granger, HJ Fazzini, A Ledda, F Univ Florence Dept Preclin & Clin Pharmacol Lab Microvasc & Cardiovasc Pharmacol Florence Italy Texas A&M Univ Syst Hlth Sci Ctr Microcirculat Res Inst College Stn TX USA Texas A&M Univ Syst Hlth Sci Ctr Dept Med Physiol College Stn TX USA

Nebivolol is a recently developed beta-blocker provided with vasodilator properties. Because the mechanism of the putative endothelium-dependent effect of this beta-adrenoceptor blocker has not been completely elucidated, the aim of this study was to investigate the effects of nebivolol on an isolated resistance vascular bed and on cell messengers and constitutive nitric-oxide synthase activity (cNOS) in endothelial cells. Experiments were carried out using the rat mesenteric vascular bed and cultured bovine coronary postcapillary venular endothelial cells from bovine heart (CVEC). In mesenteric vascular bed preconstricted by 30 mu M noradrenaline and 0.3 mu M U46619, dl-nebivolol induced a concentration-dependent relaxing effect at concentrations between 3 and 30 mu M;this effect was changed to a concentration-dependent vasoconstrictor response either in endothelium-denuded preparations or in intact preparations pretreated with 100 mM N-omega-nitro-L-arginine methyl ester plus 3 mu M indomethacin. The vasorelaxant effect of dl-nebivolol in preconstricted preparations was completely blocked by pretreatment either with the phospholipase C inhibitor U73122 (1 mu M) or with the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin (1 mu M) for 30 min. The cellular level of the inositol trisphosphate metabolite inositol monophosphate in coronary postcapillary venular endothelial cells was not affected by dl-nebivolol in the concentration range 100 nM to 1 mu M, but it was concentration dependently increased after exposure for 15 min to 10 and 30 mu M dl-nebivolol. The activity of cNOS was almost doubled after a 5-min exposure to 10 mu M dl-nebivolol and was significantly impaired by thapsigargin and N-omega-nitro-L-arginine methyl ester treatment, although it was unaffected by N-omega-nitro-D-arginine methyl ester. These findings demonstrate that nebivolol, in micromolar concentrations, induces vasorelaxation through activation of inositol phosphate metabolism and st

关键词：苯吡喃类/药理学细胞培养的剂量效应关系药物内皮血管/代谢雌烯类/药理学乙醇胺类/药理学吲哚美辛/药理学肌醇磷酸类/代谢肠系膜动脉/代谢心肌/代谢 NG-硝基精氨酸甲酯/药理学一氧化氮合酶/代谢去甲肾上腺素/药理学吡咯烷酮类/药理学大鼠 Wistar 毒胡萝卜内酯/药理学时间因素血管舒张药/药理学静脉/代谢动物牛大鼠

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