巻号一覧
77 巻 (1998)
- 4 号 p. 265-
- 3 号 p. 177-
- 2 号 p. 107-
- 1 号 p. 1-
77 巻, 4 号
選択された号の論文の9件中1～9を表示しています
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Regular Papers
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Jan Ševcík, Vladimír Ruzicka, Josef Slánský, ...1998 年 77 巻 4 号 p. 265-270
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーThe relaxations mediated by the activation of 5-HT receptors in the guinea pig proximal colon were investigated. Longitudinal strips were cut from the colon segment and placed into the bath. In the presence of atropine (0.2 μM), the relaxations were evoked by adding increasing concentrations of 5-HT (1 - 100 μM). Noncumulative concentration-response curves were established in the absence and presence of either 5-HT or nitric oxide synthase (NOS) antagonists. Selective 5-HT3 antagonists tropisetron (10 and 100 nM) and ondansetron (1 μM) inhibited the relaxations and shifted the concentration-response curves to the right. Similar effects were observed in the presence of the NOS inhibitor NG-nitro-L-arginine (3.2, 10, 32 μM) and partly reversed with L-arginine (100, 320 μM). NG-nitro-D-arginine, serving as a negative control, was ineffective. The relaxations were further inhibited in the presence of the soluble guanylate cyclase blocker methylene blue (10 μM) or NO scavenger hemoglobin (32 μM). These results suggest that the 5-HT3 receptor plays a role in neurogenic relaxations of guinea pig proximal colon, which are at least partly mediated via release of NO from nerve endings.抄録全体を表示PDF形式でダウンロード (729K) -
Hideyuki Nishiwaki, Noriko Saitoh, Hideaki Nishio, Tadayoshi Takeuchi, ...1998 年 77 巻 4 号 p. 271-278
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーThe relationship between muscarinic autoinhibition and the inhibitory effect of morphine on acetylcholine (ACh) release was investigated in a longitudinal muscle with myenteric plexus (LMMP) preparation of guinea pig ileum. Morphine (10 μM) inhibited spontaneous and evoked ACh release by electrical field stimulation (EFS) at 1 Hz but not at 10 Hz. Atropine (1 μM) did not affect the resting ACh release, but it significantly increased EFS-evoked release, suggesting activation of muscarinic autoreceptors by ACh released during EFS. Only when the autoinhibition was weakened by atropine, morphine exhibited an inhibitory effect on the EFS-evoked release at 10 Hz. Bethanechol (300 μM) inhibited the EFS-evoked release at 1 Hz but not 10 Hz, suggesting that muscarinic autoreceptors are partially or almost fully activated at 1 or 10 Hz stimulation, respectively. After bethanechol treatment, morphine did not exhibit its inhibitory effect on the EFS-evoked release at 1 Hz. Naloxone (1 μM) increased spontaneous and EFS-evoked ACh release at 1 Hz but not at 10 Hz. Following treatment with atropine, naloxone also increased ACh release at 10-Hz stimulation. These results suggest that morphine and an endogenous opioid inhibit ACh release from LMMP preparations when muscarinic autoinhibition mechanism does not fully work. This inhibitory effect of morphine is discussed in relation to the calcium sensitivity of the preparations in ACh release.抄録全体を表示PDF形式でダウンロード (938K) -
Hideyuki Nishiwaki, Noriko Saitoh, Hideaki Nishio, Tadayoshi Takeuchi, ...1998 年 77 巻 4 号 p. 279-286
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーRelationship between activation of opioid receptors and muscarinic autoinhibition in acetylcholine (ACh) release from the myenteric plexus was studied in longitudinal muscle myenteric plexus (LMMP) preparations of guinea pig ileum. A mu-receptor agonist, [D-Ala2, N-Me-Phe4, Gly5-ol] enkephalin (DAMGO), at a concentration of 1 μM inhibited the ACh release evoked by electrical field stimulation (EFS) at 1 Hz but not at 10 Hz. After the muscarinic autoreceptors were blocked with atropine (1 μM), DAMGO inhibited EFS-evoked ACh release also at 10 Hz. After the autoreceptors were potently activated with muscarine (200 μM), the inhibitory effect of DAMGO at 1 Hz was abolished. A kappa-receptor agonist, U-50, 488, at 1 μM inhibited the EFS-evoked ACh release both at 1 and 10 Hz. U-50, 488 inhibited ACh release regardless of the presence of atropine or muscarine. A delta-agonist, enkephalin [D-PEN2.5] (PDPDE), did not show any significant effect. On the other hand, a selective mu-receptor antagonist, cyprodime, increased ACh release evoked by EFS at 1 Hz, but not at 10 Hz. After the autoreceptors were blocked, cyprodime increased EFS-evoked ACh release also at 10 Hz. The selective kappa-receptor antagonist, nor-binaltorphimine, did not affect ACh release in the absence or presence of atropine. The results suggest that endogenous opioid(s) inhibits ACh release by activating mu-, but not kappa- and delta-receptors in the LMMP of guinea pig ileum and that the inhibitory effect of endogenous opioid(s) in the ACh release is important when muscarinic autoinhibition mechanism does not fully work.抄録全体を表示PDF形式でダウンロード (1014K) -
Hiroshi Watanabe, Hiromichi Tsuru, Koji Yajin, Hiroko Kawamoto, Masash ...1998 年 77 巻 4 号 p. 287-292
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーWe have previously reported that there is non-adrenergic, non-cholinergic (NANC) innervation in canine nasal mucosa and that the relaxation response to electrical stimulation of the NANC nerve is mainly mediated by nitric oxide (NO). In the present study, we examined the effect of cold exposure (24°C) on nitroxidergic nerve-mediated vasodilatation in isolated canine nasal mucosa. Nasal mucosa strips, prepared from canine nasal septum and moderately precontracted with methoxamine in the presence of atropine and guanethidine, relaxed in response to transmural electrical stimulation (square pulses of 0.5-msec duration, at 5 Hz and 25 V). The degree of relaxation at 24°C (55.4±13.2% of methoxamine-induced contraction, mean±S.D., n=6) was significantly greater than that at 34°C (33.8±8.6%, n=6). This phenomenon was reversible. In contrast, the magnitude of relaxation responses to an NO donor (sodium nitroprusside of 0.1 and 1 μM) remained unchanged by cold exposure. These results suggest that the release of NO from the nitroxidergic nerve endings is augmented by cold exposure and, thus, vasodilatation of the nasal blood vessel is enhanced, thereby contributing to the swelling of the nasal mucosa in cold conditions.抄録全体を表示PDF形式でダウンロード (687K) -
Yoshihide Tatsumi, Masamichi Tanino, Tadashi Kodama, Kei Kashima, Masa ...1998 年 77 巻 4 号 p. 293-299
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーIrsogladine maleate (IM) has been used as a mucosal protective agent, whose action is partially explained as enhancement of mucosal blood flow, increase of cellular cyclic AMP and facilitation of gap-junctional intercellular communication. Effect of IM on rat gastric mucosal hydrophobicity, one of the mucosal barrier properties, was investigated, in comparison with that of 16, 16-dimethyl prostaglandin E2 (dmPGE2). IM alone had no effect on mucosal hydrophobicity and mucosal phospholipids content. dmPGE2 alone did not change mucosal hydrophobicity significantly, but remarkably increased mucosal surface-active phospholipids. Intragastric administration of absolute ethanol significantly decreased gastric mucosal hydrophobicity and mucosal phospholipids content. IM could prevent the decrease in mucosal hydrophobicity by ethanol, maintaining the surface mucus gel layer and mucosal surface phospholipids almost as non-damaged control levels, whereas dmPGE2 also prevented the decrease in mucosal hydrophobicity by ethanol, with the surface epithelium being partially exfoliated and mucosal surface-active phospholipids showing remarkable enhancement. These results suggest that IM may preserve gastric mucosal hydrophobicity against ethanol, not through enhancement of mucosal phospholipids content like prostaglandin, but possibly through its reported stabilization action to the epithelial cell lining, which may preserve the surface epithelium with the mucous gel layer containing surface-active phospholipids, a possible origin of mucosal hydrophobicity.抄録全体を表示PDF形式でダウンロード (968K) -
Takahiro Seki, Masabumi Minami, Chiaki Kimura, Tomoya Uehara, Takayuki ...1998 年 77 巻 4 号 p. 301-306
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーWe investigated the molecular basis of the discrimination between nociceptin/orphanin FQ receptor (NociR) and opioid receptors (OPRs) by bremazocine, a non-type-selective opioid ligand. Construction of several chimeric receptors between NociR and κ-opioid receptor (KOPR) and mutant NociRs followed by binding experiments with [3H]bremazocine showed that the mutation of only four amino acid residues of NociR, Ala216, Val279, Gln280 and Val281, to the amino acid residues located at the corresponding position of KOPR, Lys227, Ile290, His291 and Ile292, made it possible for the resultant mutant NociR to bind bremazocine with high affinity. Considering that these four amino acid residues are conserved among μ-, δ- and κ-OPRs, the present result suggests that bremazocine recognizes the difference in these four amino acid residues to discriminate between NociR and OPRs.抄録全体を表示PDF形式でダウンロード (871K)
Short Communications
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Lydie Auger-Pourmarin, Pierre Roubert, Pierre Etienne Chabrier1998 年 77 巻 4 号 p. 307-310
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーEndothelin receptors were characterized in rat prostate and potential modification of these receptors was investigated in prostatic hypertrophy induced by testosterone. Both ETA and ETB endothelin receptor mRNA were detected in rat prostate, whereas binding experiments show the presence of only ETA receptors. Testosterone administration produced a 75% increase in prostate weight. Although the density of prostatic endothelin receptors was decreased from 348±75.0 fmol/mg protein in control rats to 252±39.9 fmol/mg protein in testosterone-treated animals, the total amount of receptors per prostate was unchanged. The steady-state level of ETA- and ETB-receptor mRNA was not altered by testosterone treatment. These results suggest that endothelin receptors are not affected in prostatic hypertrophy induced by testosterone.抄録全体を表示PDF形式でダウンロード (542K) -
Hideo Honda, Kiyoshi Yamaguchi, Hiroshi Kogo1998 年 77 巻 4 号 p. 311-313
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーFemale Wistar rats were treated with 17β-estradiol (E2) (10 μg, s.c.) or with sesame oil for 3 days. The relaxation induced by isoproterenol (10-9-3×10-6 M) in aortae precontracted with norepinephrine was significantly suppressed in aortae from E2-treated rats compared with the relaxation in those from control rats. NG-Nitro-L-arginine, a nitric oxide synthase inhibitor, inhibited isoproterenol-induced relaxation in aortae from both E2-treated and control rats. Metyrapone, a cytochrome P-450 monooxygenase inhibitor, inhibited it in aortae from control rats, but metyrapone enhanced the maximum relaxation in aortae from E2-treated rats. These results suggest that E2 modulates isoproterenol-induced vasodilation through nitric oxide and cytochrome P-450-dependent metabolites.抄録全体を表示PDF形式でダウンロード (390K) -
Yasusuke Masuda, Tamami Oguma, Hiroko Kaneko1998 年 77 巻 4 号 p. 315-318
発行日: 1998年
公開日: 2001/04/26
ジャーナル フリーIntrahepatic flow in rats was examined by systemic acridine orange (AO) labeling and succeeding microscopic observations of post-fixed livers. In controls, all periportal areas were stained evenly throughout the liver mass, and the staining often branched between the liver lobules in a acinous fashion. Intraportal endothelin-1 infusion caused a marked heterogenous staining; strong staining around large portal vein branches in the central portion of the liver, but much less in the periphery. Cirrhotic livers exhibited overall weaker staining intensity with no accentuation in periportal areas and restricted radial staining within pseudo-lobules. AO infusion may help detect hepatic flow disturbance in vivo.抄録全体を表示PDF形式でダウンロード (684K)
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