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^99mTc-labeled MIBG derivatives:: Novel ^99mTc complexes as myocardial imaging agents for sympathetic neurons

BIOCONJUGATE CHEMISTRY 1999年第2期10卷 159-168页

作者： Zhuang, ZP Kung, MP Mu, M Hou, A Kung, HF Univ Penn Dept Radiol Philadelphia PA 19104 USA Univ Penn Dept Pharmacol Philadelphia PA 19104 USA

Radioactive-iodine-labeled meta-iodobenzylguanidine (MIBG) is currently being used as an in vivo imaging agent to evaluate neuroendocrine tumors as well as the myocardial sympathetic nervous system in patients with myocardial infarct and cardiomyopathy. It is generally accepted that MIBC;is an analogue of norepinephrine and its uptake in the heart corresponds to the distribution of norepinephrine and the density of sympathetic neurons. A series of MIBG derivatives containing suitable chelating functional groups N2S2 for the formation of [(TcO)-O-v]3+N2S2 complex was successfully synthesized, and the Tc-99m-labeled complexes were prepared and tested in rats. One of the compounds, [Tc-99m]2, tested showed significant, albeit lower, heart uptakes post iv injection in rats (0.21% dose/g at 4 h) as compared to [I-125]MIBG (1.7% dose/g at 4 h). The heart uptake of the Tc-99m-labeled complex appears to be specific and can be reduced by co-injection with nonradioactive MIBG or by pretreatment with desipramine, a selective norepinephrine transporter inhibitor. Further evaluation of the in vitro uptake of [Tc-99m]2 in cultured neuroblastoma cells displayed consistently lower, but measurable uptake (approximately 10% of that for [I-125]MIBG). These preliminary results suggested that the mechanisms of heart uptake of [Tc-99m]2 may be related to those for [I-125]MIBG uptake. If suitable Tc-99m-labeled MIBG derivatives can be further developed, the prevalent availability of Tc-99m in nuclear medicine clinics will allow them to be readily available for widespread application.

关键词：心脏/神经支配心脏/放射性核素显像指示剂和试剂心肌/代谢神经母细胞瘤放射性药物/化学合成放射性药物/诊断应用放射性药物/药代动力学大鼠 Sprague-Dawley 构效关系交感神经系统/代谢交感神经系统/放射性核素显像锝/诊断应用锝/药代动力学组织分布肿瘤细胞培养的动物人类男(雄)性大鼠

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NEW APPROACHES TO EVALUATE SYMPATHOADRENAL SYSTEM ACTIVITY IN EXPERIMENTS ON EARTH AND IN-SPACE

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ACTA ASTRONAUTICA 1994年第C期34卷 243-254页

作者： KVETNANSKY, R NOSKOV, VB BLAZICEK, P MACHO, L GRIGORIEV, AI GOLDSTEIN, DS KOPIN, IJ National Institutes of Health NINDS Bethesda Maryland USA

In previous studies the activity of the sympathoadrenal system (SAS) in cosmonauts during space flights was evaluated by measuring plasma catecholamines (CA) levels and urinary CA and their metabolites concentrations. Plasma CA levels are accepted indicators of SAS activity, however, they are determined by the plasma clearances as well as the rates of CA release (spillover-SO) into the bloodstream. Nowadays methods are available which evaluate not only plasma levels of CA but also their release, spillover, uptake, reuptake, degradation and also CA synthesis in vivo measured by plasma levels of dihydroxyphenylalanine (DOPA). Plasma concentrations of DOPA, the CA noradrenaline (NE), adrenaline (ADR), and dopamine (DA), the deaminated catechol metabolites dihydroxyphenylglycol (DHPG) and dihydroxyphenylacetic acid (DOPAC), and the O-methylated metabolites methoxyhydroxyphenylglycol (MHGP) and homovanillic acid (HVA) were measured during immobilization stress (IMO) in conscious rats. Radiotracer methods were used to measure NE SO. IMO markedly increased arterial NE levels but NE SO was less elevated because the NE clearance was slightly reduced in IMO rats. Simultaneous measurements of plasma CA and their metabolites provide another means to obtain information about SAS function. For instance, dissociation between changes of plasma DHPG and NE levels can indicate changes in neuronal reuptake of NE. We found marked parallel increases in plasma NE and DHPG levels during acute IMO;however after repeated IMO, plasma NE levels were increased but DHPG responses were less pronounced suggesting a reduced NE reuptake. DOPA, the CA precursor, circulates in plasma at a concentration higher than NE. During stress, increased sympathoneural outflow stimulates DOPA synthesis and release into the circulation supporting the view that changes in plasma DOPA levels during stress reflect in vivo changes in the rate of CA synthesis. We propose to measure the new plasma indicators of SAS act

关键词： 3 4-二羟苯酰乙酸/血液 3 4-二羟苯酰乙酸/代谢航天医学宇航员儿茶酚胺类/血液儿茶酚胺类/代谢二羟苯丙氨酸/血液二羟苯丙氨酸/代谢多巴胺/血液多巴胺/代谢肾上腺素/血液肾上腺素/代谢高香草酸/血液高香草酸/代谢甲氧基羟基苯乙二醇/类似物和衍生物甲氧基羟基苯乙二醇/血液甲氧基羟基苯乙二醇/代谢去甲肾上腺素/血液去甲肾上腺素/代谢大鼠 Sprague-Dawley 血清素激动药/药理学宇宙飞行应激/血液应激/病因学应激/代谢交感神经系统/代谢交感神经系统/生理学失重 α甲基酪氨酸/药理学动物人类男(雄)性大鼠

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Role of apoptosis signal-regulating kinase in regulation of the c-Jun N-terminal kinase pathway and apoptosis in sympathetic neurons

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MOLECULAR AND CELLULAR BIOLOGY 2000年第1期20卷 196-204页

作者： Kanamoto, T Mota, M Takeda, K Rubin, LL Miyazono, K Ichijo, H Bazenet, CE Japanese Fdn Canc Res Inst Canc Dept Biochem Toshima Ku Tokyo 170 Japan Hiroshima Univ Sch Med Dept Ophthalmol Minani Ku Hiroshima 734 Japan Tokyo Med & Dent Univ Fac Dent Dept Biomat Sci Bunkyo Ku Tokyo 1138549 Japan UCL EISAI London Res Labs London WC1E 6BT England Ontogeny Inc Cambridge MA 02319 USA

We have previously shown that nerve growth factor (NGF) withdrawal-induced death requires the activity of the small GTP-binding protein Cdc42 and that overexpression of an active form of Cdc42 is sufficient to mediate neuronal apoptosis via activation of the c-Jun pathway. Recently, a new mitogen-activated protein (MAP) kinase kinase kinase, apoptosis signal-regulating kinase 1 (ASK1) which activates both the c-Jun N-terminal kinase (JNK) and p38 MAP kinase pathways and plays pivotal roles in tumor necrosis factor- and Fas-induced apoptosis, has been identified. Therefore, we investigated the role of ASK1 in neuronal apoptosis by using rat pheochromocytoma (PC12) neuronal cells and primary rat sympathetic neurons (SCGs). Overexpression of ASK1-Delta N, a constitutively active mutant of ASK1, activated JNK and induced apoptosis in differentiated PC12 cells and SCG neurons. Moreover, in differentiated PC12 cells, NGF withdrawal induced a four- to fivefold increase in the activity of endogenous ASK1, Finally, expression of a kinase-inactive ASK1 significantly blocked both NGF withdrawal- and Cdc42-induced death and activation of c-jun. Taken together, these results demonstrate that ASK1 is a crucial element of NGF withdrawal-induced activation of the Cdc42-c-Jun pathway and neuronal apoptosis.

关键词：细胞凋亡细胞分化细胞培养的 JNK丝裂原活化蛋白激酶类 MAP激酶激酶激酶5 MAP激酶激酶激酶类/代谢 MAP激酶信号系统丝裂原激活蛋白激酶类/代谢神经元/代谢神经元/病理学大鼠 Sprague-Dawley 信号传导交感神经系统/代谢交感神经系统/病理学 cdc42GTP结合蛋白质/代谢动物大鼠

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Prejunctional muscarinic receptor modulation of noradrenaline release from sympathetic neurones in rabbit aorta

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PHARMACOLOGY & TOXICOLOGY 2000年第6期86卷 264-269页

作者： Lomholt, M Nedergaard, OA Odense Univ Dept Pharmacol DK-5000 Odense C Denmark

The prejunctional muscarinic modulation of stimulation-evoked release of H-3-noradrenaline from sympathetic neurones in rabbit aorta was examined. The role of transmitter uptake, alpha-adrenoceptor blockade, stimulation frequency and endothelium on the modulation was investigated. Rings of aorta were incubated with (-)-H-3-noradrenaline and subsequently subjected to electrical-field stimulation. Fractional H-3-overflow was determined by liquid scintillation counting. Acetylcholine (10(-8)-3x10(-6) M) added cumulatively, reduced the stimulation-evoked 3H-overflow up to 80%. The effect of acetylcholine was the same in intact and endothelium-free aorta. The inhibitory effect of acetylcholine was inversely related to the frequency of stimulation (1-10 Hz). The maximal inhibition (%) was 80 (1 Hz), 53 (3 Hz) and 14 (10 Hz). The inhibitory effect of acetylcholine (10(-6) M) and carbachol (10(-5) M) reached a maximum 15 min. after addition and then remained almost constant. Cocaine (3x10(-5) M) did not alter the effect of acetylcholine. Desipramine (10(-6) M) and corticosterone (4x10(-5) M) attenuated the inhibition seen with low concentrations (10(-8)-10(-7) M) of acetylcholine. The acetylcholine-induced inhibition was antagonized by desipramine. Cocaine plus corticosterone attenuated the inhibition seen with high concentrations (10(-6)-3 x 10(-6) M) of acetylcholine. Rauwolscine (10(-6) M) enhanced the maximal inhibitory effect of acetylcholine. We conclude that the inhibitory effect of acetylcholine on H-3-overflow from rabbit aorta preloaded with H-3-noradrenaline is (1) inversely related to stimulation frequency;(2) independent of endothelium;(3) unaffected by neuronal and extraneuronal transmitter uptake;(4) that cocaine is not a prejunctional muscarinic antagonist;(5) that cocaine, but not desipramine, is suited as a neuronal uptake inhibitor in studies of prejunctional muscarinic receptor subtypes;and (6) and that there is an inverse interaction between prejunction

关键词：乙酰胆碱/药理学主动脉胸/药物作用主动脉胸/神经支配主动脉胸/代谢卡巴胆碱/药理学可卡因/药理学皮质酮/药理学地昔帕明/药理学药物相互作用电刺激神经元/药物作用神经元/代谢去甲肾上腺素/代谢受体毒蕈碱/药物作用受体毒蕈碱/代谢受体突触前/药物作用受体突触前/代谢交感神经系统/药物作用交感神经系统/代谢动物女(雌)性男(雄)性兔

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RAPID TRANSPORT OF NORADRENALINE IN ADRENERGIC AXONS OF RAT SCIATIC-NERVE DISTAL TO A CRUSH

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ACTA PHYSIOLOGICA SCANDINAVICA 1975年第3期94卷 386-392页

作者： HAGGENDAL, J DAHLSTROM, A LARSSON, PA UNIV GOTHENBURG DEPT PHARMACOLGOTHENBURGSWEDEN UNIV GOTHENBURG INST NEUROBIOLGOTHENBURGSWEDEN

The transport of NA in the rat sciatic nerve distal to a crush was studied in 5 mm segments. The disappearance of a NA fraction in consecutive segments with time after crushing (0-12 h) was interpreted to indicate a proximo-distal migration of a NA fraction into further distal parts of the nerve. This transportable NA fraction was found to be about 45% of the NA in normal sciatic nerves and migrated at a rate of approximately 8 mm/h. The apparently non-mobile fraction (55%) was probably mainly located in vaso-constrictor nerve terminals of the blood vessels supplying the nerve. This non-mobile NA fraction does not contribute to the NA accumulations proximal to a crush. Thus, when calculating the rate of transport of any substance from accumulation experiments, corrections for a non-mobile fraction must always be considered.

关键词：轴突/代谢生物转运神经压碾神经末梢/代谢去甲肾上腺素/代谢坐骨神经/代谢交感神经系统/代谢动物男(雄)性大鼠

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IDENTIFICATION OF MUCOPOLYSACCHARIDES IN CATECHOLAMINE-CONTAINING SUBCELLULAR PARTICLE FRACTIONS FROM VARIOUS RAT, CAT AND OX TISSUES

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ACTA PHYSIOLOGICA SCANDINAVICA 1976年第1期97卷 110-120页

作者： BLASCHKE, E BERGQVIST, U UVNAS, B KAROLINSKA INST DEPT PHARMACOL S-10401 STOCKHOLM 60 SWEDEN

Subcellular fractions containing adrenergic vesicles were obtained from bovine adrenal medulla and splenic nerve, rat and cat heart and rat spleen. The fractions were washed free from lipids, digested with papain, and the mucopolysaccharides (MPS) then precipitated from the supernatant with ethanolic potassium acetate. The MPS were identified by several different methods: microelectrophoresis on cellulose acetate in various media, cellulose column chromatography using elution solvents of increasing ionic strength and treatment with specific enzymes followed by electrophoresis or column chromatography. The MPS precipitate from all the sources investigated contained dermatan sulfate or a dermatan sulfate-chondroitin sulfate hybrid. The precipitate from rat spleen contained chondroitin sulfate. Heparan sulfate was found in the precipitates from rat heart and spleen and hyaluronic acid in that from bovine splenic nerve. The finding of sulfomucopolysaccharides in the adrenergic vesicles, probably in a complex with protein, raises the question of the functional significance of such complexes. They might, by analogy with the ion-exchange function of the heparin-protein complex in mast cell granules, play a role in the storage and release of the amines.

关键词：肾上腺髓质/代谢儿茶酚胺类/分析儿茶酚胺类/代谢葡糖氨基聚糖类/分离和提纯葡糖氨基聚糖类/代谢心肌/代谢去甲肾上腺素/分析去甲肾上腺素/代谢种特异性脾/代谢亚细胞部分/分析亚细胞部分/代谢硫糖神经鞘类脂/分析交感神经系统/分析交感神经系统/代谢动物猫牛大鼠

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Sympathetic nervous system, adrenergic receptors, and obesity

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JOURNAL OF LABORATORY AND CLINICAL MEDICINE 1999年第1期134卷 4-6页

作者： Bray, GA Pennington Biomed Res Ctr Baton Rouge LA 70808 USA

The article by Flechtner-Mors et al in this issue of the Journal has expanded our basis for understanding the role of the SNS and adrenergic receptors in the control of lipolysis by subcutaneous fat cells. Using microdialysis cannulas inserted into abdominal and femoral adipose tissue, they examined lipolysis by measuring glycerol release both basally and in response to locally microinfused epinephrine; to an α-adrenergic antagonist, phentolamine; to a β-adrenergic agonist, propranolol. Epinephrine increased lipolysis in both the abdominal and gluteal fat deposits, with women showing a greater response than men. The blockade of α-adrenergic receptors enhanced lipolysis, but propranolol did not significantly affect lipolysis, suggesting that in the basal state lipolysis is modulated mainly by inhibitory control through α-adrenergic receptors.

关键词：脂肪组织/神经支配脂肪组织/代谢脂肪组织/病理生理学脂解作用去甲肾上腺素/生理学去甲肾上腺素/尿肥胖症/代谢肥胖症/病理生理学受体肾上腺素能/生理学交感神经系统/代谢交感神经系统/病理生理学动物女(雌)性人类男(雄)性

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Nitric-oxide synthase-containing nerves facilitate adrenergic transmitter release in sheep middle cerebral arteries

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期293卷 397-402页

作者： Mbaku, EN Zhang, LB Duckles, SP Buchholz, J Loma Linda Univ Sch Med Dept Physiol & Pharmacol Loma Linda CA 92350 USA Univ Calif Irvine Coll Med Dept Pharmacol Irvine CA 92717 USA

Cerebral blood vessels contain both sympathetic and nitric oxide (NO) synthase (NOS)-containing nerves. NO has been proposed to modulate smooth muscle function and adrenergic nerve activity, and the nature of this modulation is controversial: some data show NO inhibits norepinephrine (NE) release, whereas others suggest that NO augments release. To test the hypothesis that in cerebral arteries NO released by NOS-containing nerves augments stimulation-evoked NE release, we used direct measurement of NE and NO release in isolated sheep middle cerebral arteries. The facial artery, which has not been reported to be innervated with NOS-containing nerves, was used as an artery comparison model. HPLC and redox electrochemical detection was used to measure NE, and NO was measured by chemiluminescence. Stimulation-evoked NE release from the middle cerebral artery significantly declined in the presence of the NOS inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME). The effect of L-NAME was reversed by the addition of the NO donor S-nitroso-N-acetyl-DL-penicillamine. In contrast, in facial arteries, L-NAME had no effect on stimulation-evoked NE release, whereas S-nitroso-N-acetyl-DL-penicillamine still significantly elevated NE release. Activation of perivascular nerves significantly increased NE release in both the middle cerebral and facial arteries. However, when NO was measured in the same samples, stimulation-evoked release of NO was significantly increased compared with basal release only in middle cerebral arteries. These data support the concept that cerebral arteries in the sheep contain both adrenergic and NOS-containing nerves. Furthermore, this study provides succinct evidence that NO released from NOS nerves augments stimulation-evoked NE release.

关键词：动脉/细胞学动脉/药物作用动脉/代谢电刺激酶抑制剂/药理学大脑中动脉/药物作用大脑中动脉/神经支配大脑中动脉/代谢 NG-硝基精氨酸甲酯/药理学神经递质药/代谢一氧化氮/代谢一氧化氮供体/药理学一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢一氧化氮合酶Ⅰ型去甲肾上腺素/代谢青霉胺/类似物和衍生物青霉胺/药理学 S-亚硝基-N-乙酰基青霉胺绵羊交感神经系统/药物作用交感神经系统/代谢动物女(雌)性

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Cyclosporine A-induced hypertension involves synapsin in renal sensory nerve endings

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第17期97卷 9765-9770页

作者： Zhang, WG Li, JL Hosaka, M Lanz, R Shelton, JM Albright, GM Richardson, JA Südhof, TC Victor, RG Univ Texas SW Med Ctr Dept Internal Med Dallas TX 75390 USA Univ Texas SW Med Ctr Dept Mol Genet Dallas TX 75390 USA Univ Texas SW Med Ctr Ctr Basic Neurosci Dallas TX 75390 USA Univ Texas SW Med Ctr Dept Pathol Dallas TX 75390 USA Univ Texas SW Med Ctr Howard Hughes Med Inst Dallas TX 75390 USA

The calcineurin inhibitor cyclosporine A (CsA) has emerged as a major cause of secondary hypertension in humans, but the underlying pathogenetic mechanisms have remained enigmatic. Synapsins are a family of synaptic vesicle phosphoproteins that are essential for normal regulation of neurotransmitter release at synapses. In addition to synaptic vesicles, synapsins and other vesicle proteins are found on microvesicles in sensory nerve endings in peripheral tissues. However, the functions of the sensory microvesicles in general, and of synapsins in particular, are unknown. We now demonstrate in a mouse model that CsA raises blood pressure by stimulating renal sensory nerve endings that contain synapsin-positive microvesicles. In knockout mice lacking synapsin I and II, sensory nerve endings are normally developed but not stimulated by CsA whereas a control stimulus, capsaicin, is fully active. The reflex activation of efferent sympathetic nerve activity and the increase in blood pressure by CsA seen in control are greatly attenuated in synapsin-deficient mice. These results provide a mechanistic explanation for CsA-induced acute hypertension and suggest that synapsins could serve as a drug target in this refractory condition. Furthermore, these data establish evidence that synapsin-containing sensory microvesicles perform an essential role in sensory transduction and suggest a role for synapsin phosphorylation in this process.

关键词：传入通路/药物作用传入通路/代谢血压/药物作用辣椒辣素/药理学环孢菌素/代谢环孢菌素/药理学疾病模型动物高血压/化学诱导高血压/代谢免疫组织化学嗜免疫剂/代谢肾/药物作用肾/神经支配配体小鼠近交C57BL 小鼠基因敲除神经末梢/药物作用神经末梢/代谢神经元传入/药物作用神经元传入/代谢 P物质/分析交感神经系统/细胞学交感神经系统/药物作用交感神经系统/代谢突触蛋白类/缺乏突触蛋白类/遗传学突触蛋白类/代谢突触小泡/药物作用突触小泡/代谢 rab3AGTP结合蛋白质/分析动物女(雌)性男(雄)性小鼠

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EFFECTS OF MYOCARDIAL-INFARCTION ON ADRENERGIC NERVES OF RAT-HEART MUSCLE, A HISTOCHEMICAL STUDY

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ACTA PHYSIOLOGICA SCANDINAVICA 1975年第3期93卷 336-344页

作者： AHONEN, A HARKONEN, M JUNTUNEN, J KORMANO, M PENTTILA, A UNIV HELSINKI DEPT FORENSIC MEDHELSINKIFINLAND UNIV TURKU DEPT DIAG RADIOLTURKUFINLAND UNIV HELSINKI DEPT ANATHELSINKIFINLAND

The anterior branch of the left coronary artery of the rat heart was ligated and the effects of anoxia on adrenergic nerves were studied histochemically using formaldehyde-induced fluorescence for localization of norepinephrine. Greenish catecholamine fluorescence was associated in the normal or infarcted myocardium only with adrenergic nerves. Constant but not prominent changes were seen in adrenergic nerve fibers 2 or 4 h after ligation of the coronary artery; the number of dilicate adrenergic fibers was reduced and some diffusion of the histochemical reaction was seen in small areas of the infarcted myocardium. Strong effects of anoxia were seen 8 h or more after ligation of the coronary artery. These were characterized by a prominent diffusion of the histochemical reaction and gradual disappearance of adrenergic structures in 2 to 4 days of anoxia. During the healing phase the appearance of numerous adrenergic nerve fibers was closely connected with the ingrowth of a new vascular bed into the infarction area. The observations indicate that adrenergic nervous structures of the myocardium resist the effects of anoxia, which may indicate the viability of sympathetic nerves in the infarcted area during long periods of anoxia.

关键词：缺氧儿茶酚胺类/代谢冠状血管心室/病理学结扎术显微镜检查荧光心肌梗死/代谢心肌梗死/病理学心肌/代谢心肌/病理学磷酸化酶类/代谢交感神经系统/代谢交感神经系统/病理学时间因素动物女(雌)性大鼠

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