巻号一覧
84 巻 (2000)
- 4 号 p. 367-
- 3 号 p. 229-
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84 巻, 4 号
選択された号の論文の17件中1～17を表示しています
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Review
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Donald B. Hoover, Yingzi Chang, John C. Hancock, Lili Zhang2000 年 84 巻 4 号 p. 367-373
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーSubstance P and neurokinin A are tachykinins that are co-localized with calcitonin gene-related peptide (CGRP) in a unique subpopulation of cardiac afferent nerve fibers. These neurons are activated by nociceptive stimuli and exhibit both sensory and motor functions that are mediated by the tachykinins and/or CGRP. Sensory signals (e.g., cardiac pain) are transmitted by peptides released at central processes of these neurons, whereas motor functions are produced by the same peptides released from peripheral nerve processes. This review summarizes our current understanding of intracardiac actions of the tachykinins. The major targets for the tachykinins within the heart are the intrinsic cardiac ganglia and coronary arteries. Intrinsic cardiac ganglia contain cholinergic neurons that innervate the heart and coronary vasculature. Tachykinins can stimulate NK3 receptors on these neurons to increase their excitability and evoke spontaneous firing of action potentials. This action provides a mechanism whereby tachykinins can indirectly influence cardiac function and coronary tone. Tachykinins also have direct effects on coronary arteries to decrease or increase tone. Stimulation of NK1 receptors on the endothelium causes vasodilation mediated by nitric oxide. This effect is normally dominant, but NK2 receptor-mediated vasoconstriction can also occur and is augmented when NK1 receptors are blocked. It is proposed that these ganglion stimulant and vascular actions are manifest by endogenous tachykinins during myocardial ischemia.抄録全体を表示PDF形式でダウンロード (618K)
Full Papers
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Masato Sakaguchi, Shinji Takai, Denan Jin, Mayumi Yamada, Mizuo Miyaza ...2000 年 84 巻 4 号 p. 375-380
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーTryptase purified from rat and dog tissues has been reported, although the characteristics of these enzymes are different from human tryptase. For pathophysiological studies of human tryptase, studies on species that have a similar tryptase to humans is needed. In this study, we purified monkey tryptase from cheek pouch vascular tissues using heparin affinity and gel filtration columns. The monkey tryptase, which had a molecular weight of 130 kDa by gel filtration, consisted of a tetramer of 33 kDa by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The N-terminal sequence showed high homology with tryptases from other species. The optimum pH and temperature were 7.5—9.0 and 25—40°C, respectively. The enzyme was labile in high-KCl buffer, and the optimum KCl concentration was 0.1 M. The enzyme activity was completely inhibited by diisopropyl phosphorofluoridate and leupeptin but not by soybean trypsin inhibitor and α-antitrypsin. The enzyme hydrolyzed vasoactive intestinal peptide but did not affect angiotensin I, somatostatin and bradykinin. In the present study, we first isolated monkey tryptase from cheek pouch vascular tissues and showed that the characteristics of monkey tryptase are very similar to those of human tryptase.抄録全体を表示PDF形式でダウンロード (422K) -
Hitoshi Kontani, Toshitsugu Tsuji, Satoko Kimura2000 年 84 巻 4 号 p. 381-390
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーWe investigated the effects of the adrenergic α2-receptor agonists clonidine, oxymetazoline and tizanidine on bladder contractions induced by infusing fluid into the bladders of conscious male rats. I.v. clonidine and oxymetazoline (both 0.01 to 0.1 mg/kg) caused bladder hyperactivity, expressed by shortening of the intercontraction interval. Tizanidine (0.1 mg/kg, i.v.) caused slight shortening of the intercontraction interval. The rank order of potency was clonidine=oxymetazoline >> tizanidine. Intrathecal (i.t.) injection of 10 μg clonidine and oxymetazoline, and intracerebroventricular (i.c.v) injection at 15 μg, produced almost the same pattern of bladder hyperactivity as that observed after i.v. injection of these drugs (0.03 mg/kg, i.v.). For all three administration routes of clonidine and oxymetazoline, i.v. idazoxan (0.3 mg/kg) exerted an inhibitory effect on the bladder hyperactivity induced by these drugs, except i.c.v injection of oxymetazoline. I.t. phenylephrine (30 μg) did not change the intercontraction interval. Although i.c.v. phenylephrine (15 μg) shortened the intercontraction interval, the potency was weaker than those of i.c.v. clonidine and oxymetazoline (15 μg). These results suggest that clonidine and oxymetazoline cause bladder hyperactivity by acting at adrenergic α2 receptors in the micturition centers of the lumbosacral and supraspinal regions.抄録全体を表示PDF形式でダウンロード (613K) -
Tomoyoshi Naganuma, Mutsuko Maekawa, Toshihiko Murayama, Yasuyuki Nomu ...2000 年 84 巻 4 号 p. 391-398
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーS-Nitroso-cysteine (SNC) inhibits Ca2+-induced noradrenaline (NA) release from PC12 cells. Since SNC stimulated Ca2+ mobilization from intracellular Ca2+ pools and SNC-induced inhibition of NA release was not washed-out, SNC may modify exocytosis-related proteins that overcome Ca2+ mobilization. In the present study, we investigated the effects of SNC on exocytosis-related proteins in PC12 cells. Ionomycin stimulated NA release and increased the immunoreactivity of synaptophysin in the cytosol fraction. A 25-kDa synaptosome-associated protein (SNAP-25), which localizes to plasma membranes and vesicles, increased in the cytosol fraction after stimulation. The increases in these proteins by ionomycin were inhibited in PC12 cells treated with 0.6 mM SNC. Synaptobrevin and synapsin-1 in the cytosol fraction, and syntaxin and 43 kDa growth-associated protein in the membrane fraction were not affected by ionomycin or SNC. Incubation of each protein with SNC did not affect antibody immunoreactivity. [32P] ADP-ribosylation of GTP-binding proteins (Gi/Go) by pertussis toxin, but not Gs by cholera toxin, was inhibited in SNC-treated PC12 cells and by co-addition of SNC to the assay mixture. These findings suggest that 1) SNC inhibits translocation of vesicles containing synaptophysin and SNAP-25, and 2) SNC reacts with cysteine residues in Gi/Go, causing inhibition of ADP-ribosylation by pertussis toxin.抄録全体を表示PDF形式でダウンロード (680K) -
Yuji Odagaki, Nobuyuki Nishi, Tsukasa Koyama2000 年 84 巻 4 号 p. 399-404
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーThe stimulation of high-affinity GTPase activity through metabotropic glutamate receptors (mGluRs) was pharmacologically characterized with the use of a series of agonists for mGluRs in rat hippocampal and striatal membranes. The pharmacological profile of the response was almost identical to each other between both brain regions. Thus, the high-affinity GTPase activities were stimulated by several mGluR-related compounds with the following rank order of potency: (2S, 2′R, 3′R)-2-(2′, 3′-dicarboxycyclopropyl)glycine(DCG-IV) ≅ (2S, 1′S, 2′S)-2-(carboxycyclopropyl)glycine (L-CCG-I) > L-glutamate ≅ 2R, 4R-4-aminopyrrolidine-2, 4-dicarboxylate [(2R, 4R)-APDC] > (S)-4-carboxy-3-hydroxyphenylglycine [(S)-4C3HPG] ≅ 1S, 3R-1-aminocyclopentane-1, 3-dicarboxylate [(1S, 3R)-ACPD] > (S)-3-carboxy-4-hydroxyphenylglycine [(S)-3C4HPG] ≅ ibotenate. The negative logarithmically transformed EC50(pEC50) values of these compounds in both brain regions were significantly correlated with those reported previously in the cerebral cortical membranes (N. Nishi et al., Br. J. Pharmacol., 130, 1664-1670, 2000). On the contrary, other reagents including a selective group I mGluRs agonist, (RS)-3, 5-dihydroxyphenylglycine [(RS)-3, 5-DHPG], and selective group III mGluRs agonists such as L(+)-2-amino-4-phosphonobutylate (L-AP4) and L-serine-O-phosphate (L-SOP) had little or no effects even at the highest concentration examined. Quisqualate was also a very weak agonist in both regions. These results indicate that mGluR-mediated high-affinity GTPase activity derives from the Gi proteins associated with adenylyl cyclase inhibition through group II mGluRs, in particular the mGluR2 subtype, in rat hippocampal and striatal membranes.抄録全体を表示PDF形式でダウンロード (502K) -
Akinobu Fujita, Kimihito Tashima, Masato Nishijima, Koji Takeuchi2000 年 84 巻 4 号 p. 405-411
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーWe compared the acid secretory response to peptone in normal and streptozotocin-induced diabetic rats. Animals were injected with streptozotocin and used after 5 weeks of diabetes with blood glucose levels of >350mg/dl. Under urethane anesthesia, 2ml peptone solution (2-8%) was instilled in the stomach through an acute fistula every 30min. Peptone increased acid secretion in a concentration-dependent manner in normal rats, the maximal response being obtained at 8%. Likewise, the increased acid response was observed in diabetic rats, yet the maximal response observed at 4% was significantly greater than that in normal rats. In both cases, this response was inhibited potently by famotidine as well as YM-022 (a CCKB antagonist) and partially inhibited by atropine. Peptone increased luminal histamine and plasma gastrin levels in both normal and diabetic rats, and the former response was significantly greater in diabetic animals. The altered acid secretion and histamine output in diabetic rats were reverted by insulin treatment. Pentagastrin- but not histamine-induced acid secretion was also increased in diabetic rats. We conclude that peptone-induced acid secretion is increased in diabetic conditions. This phenomenon is insulin-dependent and associated with an enhanced release of histamine but not with an increased sensitivity of the parietal cells.抄録全体を表示PDF形式でダウンロード (569K) -
Sanyoung Niu, Che-Hui Kuo, Yehua Gan, Etsuko Nishikawa, Tetsushi Sadak ...2000 年 84 巻 4 号 p. 412-417
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーCalmodulin (CaM) is a principal multifunctional mediator of Ca2+ signaling in cells. It is reported that morphine increases CaM contents in mouse brain. However, the precise mechanism of CaM induction by morphine is unknown. We investigated the changes of CaM by opioid receptor stimulation in mRNA and protein levels. Expression of CaM was increased in dose- and time-dependent manners by morphine with RT-PCR assay in PC12 cells, and naloxone inhibited the effect of morphine. The expression was also increased with DAMGO (μ-opioid agonist), but not by DPDPE (δ) and U50488 (κ). Northern blot analysis revealed that the CaMIII gene was responsive to morphine or DAMGO. CaM protein increased by DAMGO were distributed in both soluble and membranous fractions in the cells. Taken together, the data suggest that morphine induces the expression of CaMIII gene through μ-opioid receptor stimulation.抄録全体を表示PDF形式でダウンロード (501K) -
Nicoletta Galeotti, Carla Ghelardini, Alessandro Bartolini2000 年 84 巻 4 号 p. 418-424
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーThe effect on memory processes of modulation of 5-HT1A receptor subtype was investigated in the mouse passive avoidance test. The administration of 5-HT1A-receptor antagonists NAN-190 (1-(2-methoxyphenyl)-4-[4-2-phthalimmido)butyl]piperazine) and WAY-100635 (N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinyl-cyclohexanecarboxamide) produced a dose-dependent amnesic effect comparable to that obtained with the well-known amnesic agents scopolamine and dicyclomine. Pretreatment with the 5-HT1A-receptor agonists 8-OH-DPAT ((±)-8-hydroxy-dipropylaminotetralin) and 5-CT (5-carboxamidotryptamine) dose-dependently prevented the amnesia induced by 5-HT1A antagonists, scopolamine, dicyclomine and exposure to an hypoxic environment. The antiamnesic effect exerted by 5-HT1A-receptor agonists was comparable to that produced by the nootropic drug piracetam and cholinesterase inhibitor physostigmine. At effective doses, neither 5-HT1A-receptor agonists nor 5-HT1A-receptor antagonists produced any impairment of mouse motor coordination (rota-rod test), spontaneous motility (Animex apparatus) and inspection activity (hole board). These results indicate that modulation of 5-HT1A-receptors appears to play an important role in the regulation of cognitive processes.抄録全体を表示PDF形式でダウンロード (621K) -
Jong-Seong Park, Han-Seong Jeong2000 年 84 巻 4 号 p. 425-430
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーThe effects of nitric oxide on the vestibular function recovery following unilateral labyrinthectomy were studied. Male Sprague-Dawley rats treated with N-omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, were subjected to destruction of the unilateral vestibular apparatus and spontaneous nystagmus was observed. To explore the role of nitric oxide on the potassium current, the whole cell patch clamp technique was applied on isolated medial vestibular nuclear neurons. The frequency of spontaneous nystagmus that appeared in L-NAME-treated rats was higher and maintained longer than in control animals. Potassium currents in the isolated medial vestibular nucleus were inhibited by nitric oxide liberating agents, sodium nitroprusside and S-nitroso-N-acetylpenicillamine. After blockade of calcium dependent potassium currents by high EGTA (11 mM)-containing pipette solution, sodium nitroprusside did not inhibit the outward potassium currents. 8-Bromoguanosine 3, 5-cyclic monophosphate, a membrane-permeable cGMP analogue, produced similar effects to inhibit the outward potassium currents as sodium nitroprusside. These results suggest that nitric oxide production after unilateral labyrinthectomy would help to facilitate vestibular compensation by inhibiting calcium-dependent potassium currents through increasing intracellular cyclic GMP, thereby increasing excitability in ipsilateral vestibular nuclear neurons.抄録全体を表示PDF形式でダウンロード (407K) -
Toshihiro Unno, Tadafumi Inaba, Hidenori Ohashi, Tadashi Takewaki, Sei ...2000 年 84 巻 4 号 p. 431-437
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーIn single smooth muscle cells dispersed from guinea pig ileum, the muscarinic agonist carbachol (CCh) at 2μM produced an oscillatory or sustained type of depolarization and at 100μM, the latter type depolarization. Depletion of internal Ca2+ stores blocked the oscillatory response, but not the sustained responses to 2μM and 100μM CCh, although their decay after reaching the peak became faster. Blocking voltage-dependent Ca2+ channels (VDCCs) blocked both types of response to 2μM CCh, but only slowed the initial rising phase of 100μM CCh responses. Combination of Ca2+ store depletion and VDCC blockade abolished the responses to 2μM CCh again and decreased those to 100μM CCh in peak amplitude and persistency. Combination of Ca2+ store depletion with removal of extracellular Ca2+ markedly reduced or abolished the 100μM CCh responses. The results suggest that muscarinic depolarization of the ileal cells requires Ca2+ mobilization for its generation and persistence; at weak muscarinic stimulation, both Ca2+ entry via VDCCs and Ca2+ release from internal stores may contribute to the Ca2+ mobilization; and under strong muscarinic stimulation, Ca2+ entry pathways resistant to VDCC blockers may also contribute to it.抄録全体を表示PDF形式でダウンロード (530K) -
Zhong-Fang Lai, Katsuhide Nishi2000 年 84 巻 4 号 p. 438-448
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーWe investigated effects of extracellular ATP on intracellular chloride activities ([Cl-]i) and possible contribution of the Cl--HCO3- exchange to this increase in [Cl-]i in isolated guinea pig ventricular muscles. The [Cl-]i and intracellular pH (pHi) were recorded in quiescent ventricular muscles using double-barreled ion-selective microelectrode techniques. MgATP at a concentration higher than 0.1mM, induced an increase in [Cl-]i, and this increase in [Cl-]i was dependent on the concentration of ATP but not on the concentration of magnesium ions present in the perfusion solution. NaADP, but not NaAMP, at a concentration of 0.5mM induced a similar increase in [Cl-]i as that induced by MgATP. However, the NaADP-induced increase in [Cl-]i was transient and gradually returned to the control level even though NaADP was continuously present. Furthermore, ATP also triggered a transient acidification of pHi, and both increases in [Cl-]i and intracellular H+ induced by ATP were prevented when preparations were pretreated with stilbene derivatives, SITS and DIDS, or perfused with a Cl--free solution. Our findings showed that the increased extracellular ATP concentrations might trigger an increase in [Cl-]i in ventricular muscles. In light of previous studies showing that cardiac ischemia induced increases in extracellular nucleotide concentrations and [Cl-]i in ventricular muscles, we propose that ischemia-induced accumulation of ATP concentration in the extracellular space may be an important factor to trigger increment of [Cl-]i during ischemic conditions.抄録全体を表示PDF形式でダウンロード (805K) -
Denan Jin, Shinji Takai, Mayumi Yamada, Masato Sakaguchi, Mizuo Miyaza ...2000 年 84 巻 4 号 p. 449-454
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーRecently, a chymase-dependent angiotensin (Ang) II-forming pathway was found in human cardiovascular tissues, and the significance of this pathway in the pathogenesis of some cardiovascular diseases was suggested. The present study examined the ratio of angiotensin converting enzyme (ACE) to chymase-dependent Ang II formation in various isolated vessels from monkeys, dogs and rats. In all of the examined vessels, the addition of KCl at a concentration of 50 mM could induce a maximal contraction. Except for monkey coronary artery and rat renal and femoral artery, the addition of Ang I could induce transitory contractions, whereas the force of contractions in these vessels was quite different. The sensitivity to Ang II in these vessels was similar to that for Ang I. In monkey gastroepiploic and mesenteric arteries, about 70% of the Ang I-induced contraction was suppressed by chymase inhibition, while it was suppressed about 50% in monkey renal, femoral and carotid arteries. In dog renal arteries, about 65% of the Ang I-induced contraction was suppressed by chymase inhibition, while it was suppressed by about 30% in other dog arteries. In contrast, in all rat arteries, Ang I-induced contractions were completely suppressed by treatment with ACE inhibitor alone. We concluded that regional differences in the response to Ang I exist in vascular tissues, and the ratio of ACE- to chymase-dependent Ang II formation is different in the various vessels.抄録全体を表示PDF形式でダウンロード (524K) -
Koji Yoshinaga, Masataka Washizuka, Yoshihide Segawa2000 年 84 巻 4 号 p. 455-461
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーWe examined the effects of fasting and non-fasting on gallstone-related acute pancreatitis by the occlusion of the common bile duct (OCD). We prepared a rat OCD-induced pancreatitis model under both fasting and non-fasting conditions, and we measured amylase activity in ascites as well as production of inflammatory cytokines and chemokines. We also examined the pathology of the pancreas, myeloperoxidase (MPO) activity in some tissues and mortality rates. In the fasted OCD group, ascites containing a large amount of amylase, interleukin 1β (IL-1β), interleukin 6 (IL-6), and cytokine-induced neutrophil chemoattractant-1 (CINC-1) as well as marked hemorrhage and necrosis of the pancreatic acinar cells were observed. Pulmonary MPO activity increased 3.4-fold compared to the control group. In the non-fasted OCD group, there was no development of ascites. Slight necrosis of acinar cells and slight increases in pulmonary MPO activity were observed. In addition, in the fasted OCD group, the cumulative mortality rate was 50% 6 days after ligation. However, in the non-fasted OCD group, none of the animals died. These results suggest that gallstone-related severe pancreatitis depends on fasting-related structural and/or functional changes in the pancreas. Moreover, increased production of inflammatory cytokines and chemokines in ascites under fasting condition may be involved in multiple organ failure resulting from severe acute pancreatitis.抄録全体を表示PDF形式でダウンロード (485K)
ShortCommunication
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Tatsuya Maekawa, Hiroshi Nojima, Yasushi Kuraishi2000 年 84 巻 4 号 p. 462-466
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーTo assess the itch-associated response of primary afferents innervating the murine skin in vivo, dose-response curves and time-courses for itch-scratching and cutaneous nerve firing responses to intradermal injections of pruritogens (histamine and serotonin) were compared in ICR and ddY mice. Serotonin increased the itch-scratch response and cutaneous nerve firing in either ICR or ddY mice. Histamine increased these two responses in ICR, but not ddY, mice. The dose-response curves and time-courses for serotonin- and histamine-induced nerve firing were similar to those for the itch-scratch response. The results suggest that cutaneous nerve firing evoked by peripherally given pruritogens includes the itch-associated response.抄録全体を表示PDF形式でダウンロード (339K) -
Akçahan Gepdiremen, Selma Düzenli, Ahmet Hacimüft&uum ...2000 年 84 巻 4 号 p. 467-469
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーIn the present study, melatonin was tested in subsequent doses in glutamate induced neurotoxicity in cerebellar granular cell culture of rat pups. Glutamate at 10-7M was found to induce neuronal cell death. The dead cell score was 2.75±0.7 in the control, while it was found to be 35.12±1.8 in the glutamate-administered group (P<0.0001). Melatonin very potently blocked glutamate neurotoxicity at all doses tested, with 10-3M, the highest dose tested, being the most effective. Glutamate may exert a neuroprotective effect by blocking one or more steps of the oxidation cascade in neurons and this effect may be blocked by melatonin.抄録全体を表示PDF形式でダウンロード (218K) -
Tomohisa Hirai, Hiromichi Tsuru, Noriaki Tanimitsu, Masaya Takumida, H ...2000 年 84 巻 4 号 p. 470-473
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーThe effect of hydrogen peroxide (H2O2) on guinea pig nasal mucosa vasculature was studied by in vitro assay. H2O2 elicited relaxation of guinea pig nasal mucosa strips precontracted with phenylephrine in a concentration-dependent manner. The relaxant response to H2O2 was abolished in the presence of catalase. Preincubation of the strips with NG-nitro-L-arginine methyl ester or methylene blue significantly attenuated the relaxant responses elicited by H2O2. Fluorescence caused by DAF-2 DA, a fluorescence indicator for nitric oxide, was observed along the nasal mucosa vasculature in response to H2O2. These results suggest that H2O2 induced relaxation of the guinea pig nasal mucosa vasculature and that this relaxation in mediated by the NO/cGMP pathway.抄録全体を表示PDF形式でダウンロード (259K)
Rapid Communication
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Ryo Yoshimoto, Masatoshi Hori, Katsuhito Takahashi, Shun-ichiro Tanigu ...2000 年 84 巻 4 号 p. 474-475
発行日: 2000年
公開日: 2001/05/31
ジャーナル フリーRole of h1 calponin on Ca2+-sensitivity of smooth muscle contraction was investigated using h1 calponin gene-deficient mice (CP−/−) and wild type mice (CP+/+). PGF2α induced a comparable force in intact aorta of CP+/+ and CP−/−. DPB showed similar effects to PGF2α. In membrane-permeabilized ileal smooth muscle, PDBu enhanced Ca2+-sensitivity of contraction comparably in CP+/+ and CP−/−. GTPγ-S showed similar effects. Our results suggest that h1 calponin does not regulate Ca2+-sensitivity in the contractile mechanism of smooth muscle.抄録全体を表示PDF形式でダウンロード (139K)
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