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Volume 45 (1987)
- Issue 4 Pages 439-
- Issue 3 Pages 295-
- Issue 2 Pages 129-
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Volume 45, Issue 3
Displaying 1-18 of 18 articles from this issue
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Brij L. SHARMA, Shashi KHANDELWAL, Devendra N. KACHRU, Surendra SINGH, ...1987 Volume 45 Issue 3 Pages 295-302
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSβ-1, 2-Phenylene di-α-mercaptoacrylic acid (1, 2-PDMA), β-1, 4-phenylene di-α-mercaptoacrylic acid (1, 4-PDMA) and α-mercapto-β-(2-hydroxy-phenyl) acrylic acid (MHA) were synthesized and compared with 2, 3-dimercaptopropane-1-sulfonate (DMPS) for their ability to counteract toxic effects of lead and nickel in rats. 1, 2-PDMA and DMPS were most effective in enhancing the excretion of metals, restoring most of the metal induced biochemical alterations and reducing the body burden of the metals; These observations confirm that the chelating agents with two adjacent sulfhydryl groups are better than those with non-adjacent SH groups as metal antidotes. The success of MHA in mobilizing the tissue metals and increasing their urinary excretion indicates participation of the hydroxy group on the benzene nucleus besides the SH group of the MHA molecule, in chelation of the metals.View full abstractDownload PDF (405K) -
Takashi MATSUBARA, Shigemi OTSUBO, Ayako OGAWA, Keiko KAWAMOTO, Joji O ...1987 Volume 45 Issue 3 Pages 303-315
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe disulfiram-like effect of various beta-lactam antibiotics containing N-methyltetrazolethiol (NMTT) on the alcohol-metabolizing system was studied using rats. Their administration caused decreased activities in low Km aldehyde dehydrogenase (ALDH) and acetaldehyde oxidation in the liver, with marked depression from several hours to 2 days after the treatment. Blood acetaldehyde level increased markedly when ethanol was administered 18-24 hr after pretreatment with antibiotics. A similar time course change in the effect was obtained when disulfiram was administered. The following results obtained in the present study indicate that the disulfiram-like effect associated with these antibiotics was not mediated by the whole molecular structures of these drugs: Firstly, the antibiotics were eliminated rapidly from the plasma and liver, and the disulfiram-like effect was followed by a disappearance of the drugs. Secondly, the concentration of antibiotics required to inhibit mitochondrial low Km ALDH activity in vitro was very high compared with their liver concentration. Thirdly, rapid onset of disulfiram-like effects occurred after administration of NMTT itself, and a pronounced elevation of blood acetaldehyde level was observed when ethanol was administered 3-5 hr after the NMTT injection. Fourthly, almost the same amounts of NMTT were released in the body after the intravenous administration of various NMTT-containing antibiotics, as judged by the urinary excretion. These results suggest that the disulfiram-like effect of beta-lactam antibiotics is mediated by NMTT released from them.View full abstractDownload PDF (678K) -
Shinjiro NAKAJYO, Kiyomi MATSUOKA, Tomohiro KITAYAMA, Yutaka YAMAMURA, ...1987 Volume 45 Issue 3 Pages 317-325
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSAn inhibitory effect of beauvericin, a cyclodepsipeptide, on a high K+-induced contraction in guinea-pig taenia coli was compared with those of verapamil, an organic Ca2+ antagonist, and monensin, an inhibitor of mitochondrial respiration. Beauvericin (10-5 M), verapamil (5×10-7 M) or monensin (10-6 M) markedly inhibited the tonic contraction, while these drugs showed less effect on the phasic contraction. Beauvericin at a lower concentration (10-6 M) competitively inhibited the Ca2+-induced contraction in depolarized muscle, whereas higher concentrations (3×10-6 or 10-5 M) non-competitively inhibited this contraction. Verapamil (10-8-5×10-7 M) competitively inhibited and monensin at a low concentration (10-7 M) non-competitively inhibited this contraction. A contraction induced by 0.5 mM Ca2+ was inhibited by beauvericin with an IC50 (concentration needed for 50% inhibition) of 2.8×10-7 M, verapamil with an IC50 of 2.9×10-8 M, and nifedipine with an IC50 of 1.8×10-9 M. 10-6 M CGP 28392, a Ca2+ channel facilitator, increased the IC50 of beauvericin, verapamil or nifedipine. Although the inhibitory effect of monensin (10-7-10-6 M) on the high K+-induced contraction was reduced under hypoxia, the effects of beauvericin (10-7-10 -5 M) and verapamil (10-8-10-7 M) were not modified. Beauvericin (10-5 M) changed neither the intracellular Na+ and K+ contents of the depolarized muscle nor the Ca2+-induced contraction in the chemically skinned taenia coll. These results suggest that the inhibitory action of beauvericin (10-5 M) on the high K+-induced tonic contraction is due to the non-competitive inhibition of Ca2+ entry through the voltage-dependent Ca2+ channel of the intestinal smooth muscle cell.View full abstractDownload PDF (456K) -
Tomochika OHNO, Momoyo NAKAGAWA, Seiichiro NISHIMURA, Koji TAKEUCHI, S ...1987 Volume 45 Issue 3 Pages 327-334
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSProstaglandins protect against the gross damage of gastric mucosa induced by 50-100% ethanol, but do not protect surface epithelial cells (SEC) from necrosis. Since this induced damage to SEC is so severe, we attempted to determine the effects of a prostaglandin on slightly induced SEC damage and gastric potential difference (PD) in response to low concentrations of ethanol. The necrotizing effects of graded concentrations of ethanol (10-50%) to SEC on the rat gastric mucosa were studied by scanning electron and light microscopy. Intragastric instillation of 20% ethanol (v/v, 1 ml/100 g body wt.) to pylorus-ligated rats for 10 min induced slight and reproducible SEC damage consisting mainly of the apical cell membrane erosion of SEC. Pretreatment with 16, 16-dimethyl prostaglandin E2 (dmPGE2, 3 or 30 μg/kg, p.o. or s.c.) afforded protection of the SEC from 20% ethanol-induced damage. However, the cytoprotective effects of dmPGE2 were abolished when gastric contents were emptied prior to 20% ethanol instillation. Intragastric instillation of ethanol immediately reduced PD in a concentration-related manner. dmPGE2 (3 or 30 μg/kg, s.c.) had no effect on the reduction of gastric PD after 20% ethanol treatment and the recovery of reduced PD to normal levels. We conclude that dmPGE2 has no cytoprotective effect on 20% ethanol-induced SEC damage in rat gastric mucosa.View full abstractDownload PDF (644K) -
Syunji YOKOTA, Yoshiyuki ISHIKURA, Hiroshi ONO1987 Volume 45 Issue 3 Pages 335-342
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe cardiovascular effects of various antidepressant drugs including paroxetine, imipramine, amitriptyline and clomipramine, administered intravenously, have been assessed. Paroxetine, imipramine, amitriptyline or clomipramine potentiated the response to norepinephrine (0.1 μg/kg, i.v.) on systemic blood pressure, while paroxetine, imipramine and amitriptyline weakened the response to tyramine (30 μg/kg, i.v.). A marked decrease in systemic blood pressure was observed after large doses of each drug (3 and 10 mg/kg of paroxetine; 1-10 mg/kg of imipramine, amitriptyline or clomipramine); and half of the animals died following administration of 10 mg/kg of imipramine, amitriptyline or clomipramine. Paroxetine did not show a marked effect on heart rate at a dose of up to 3 mg/kg, although 0.13 mg/kg of imipramine, amitriptyline or clomipramine dose-dependently caused tachycardia. ECG disturbances were observed in animals administered 10 mg/kg of imipramine, amitriptyline or clomipramine; but in contrast, 10 mg/kg of paroxetine caused only slight changes in the ECG. Prolongation of atrio-ventricular conduction time was observed with all the drugs. It was concluded that the effects of paroxetine on the canine heart are more mild in comparison with other tricyclic antidepressants used, although its pharmacological features are essentially similar to those of other drugs.View full abstractDownload PDF (487K) -
Haruko SUGINO, Hideyo SHIMADA1987 Volume 45 Issue 3 Pages 343-348
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffect of isoproterenol on renal uric acid excretion was examined in oxonate-loaded and oxonate-nonloaded rats, using a clearance technique. Oxonate loading was performed by continuous infusion into the femoral vein. Isoproterenol (50 μg/kg, i.v.) induced antidiuresis and hyperuricemia accompanied with decreases in urinary excretion rate of uric acid, uric acid clearance, inulin clearance, and uric acid clearance/inulin clearance ratio in oxonate-nonloaded rats. These effects of isoproterenol were inhibited by propranolol (1 mg/kg, i.v.). Very similar results were obtained in oxonate-loaded rats; i.e., systemic blood pressure decreased synchronously with uric acid excretion by isoproterenol. In contrast, phenylephrine (100 μg/kg, i.v.) induced hypertensive, diuretic and slightly uricosuric results. In allopurinol-pretreated and oxonate-loaded rats, isoproterenol also decreased renal uric acid excretion and showed a less potent hyperuricemic effect than that observed in the animals not pretreated with allopurinol. In addition, in rats with ligated renal vessels, the hyperuricemic effect of isoproterenol was completely inhibited by allopurinol. These results suggest that isoproterenol-induced hyperuricemia is related not only to the stimulation of uric acid production, but also to the depression of renal uric acid excretion.View full abstractDownload PDF (318K) -
Hiroshi TSUCHIHASHI, Junichiro AONO, Takafumi NAGATOMO, Tomie KAWADA, ...1987 Volume 45 Issue 3 Pages 349-356
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSTo assess the importance of anti-adrenergic and anti-serotonergic activities of bunitrolol for its efficacy as an antihypertensive and antianginal agent, effects of this substance on the binding of adrenergic and serotonergic agents to the respective receptors of the rat brain, rat heart, dog brain, and/or dog aorta were examined using the radioligand binding assay methods. In addition, the pA2 values of bunitrolol as an antagonist against the positive chronotropic and inotropic actions (β1-adrenoceptor) of isoproterenol were also determined by pharmacological methods using the isolated guinea pig atria. To assess the specificity, pA2 values were also obtained in the isolated trachea (β2-adrenoceptor) using isoproterenol as an agonist and in the isolated aorta from the guinea pig and the rat using phenylephrine as an agonist (α1-adrenoceptor). A strong inhibition by bunitrolol of 3H-dihydroalprenolol (3H-DHA) binding to β-adrenoceptors was observed, while the inhibition of 3H-prazosin binding to α1-adrenoceptors, 3H-serotonin binding to 5HT1-receptors. 3H-p-aminoclonidine binding to α2-adrenoceptors, and 3H-ketanserin binding to 5HT2-receptors were found to be very weak. The rank order of antagonistic potencies of bunitrolol against the adrenergic receptors as asessed with pA2 values were β1>β2>>α1. From these two different types of experiments, it is clear that the antihypertensive and antianginal effects of bunitrolol are mainly due to its β-blocking actions, with the α1-blocking action of this drug playing a minor role.View full abstractDownload PDF (403K) -
Masanobu URABE, Hiromu KAWASAKI, Koichiro TAKASAKI1987 Volume 45 Issue 3 Pages 357-364
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effect of methamphetamine, an indirectly acting sympathomimetic amine, on presynaptic adrenergic regulation in isolated rat vas deferens was studied by comparing it with those of tyramine, cocaine and clonidine. These drugs markedly attenuated the twitch response to electrical field stimulation in a concentration-dependent manner. The relative order of potency for the drugs was: clonidine (10-10-3×10-8 M) > methamphetamine (10-8-3×10-6 M) > tyramine (10-7-10-4 M) > cocaine (10-6-3×10-5 M). Only tyramine (3×10-6-10-4 M) elicited a concentration-dependent contractile response, which was abolished by prazosin (10-6 M) and the reserpinization. The twitch inhibitory effect of these drugs was antagonized by yohimbine (10-8-10-6 M). Both the methamphetamine- and tyramine-induced twitch inhibition were partially (about 50%) attenuated by chronic reserpinization (3 mg/kg, s.c., twice) in combination with alpha-methyl-p-tyrosine (200 mg/kg, s.c., twice), while the clonidine-induced inhibition was not affected by this application at all, and the cocaine-induced twitch inhibition was abolished by the reserpinization. Both the clonidine- and tyramine-induced twitch inhibition were not affected by pretreatment with cocaine (10-5 M) in combination with estradiol (4×10-5 M), whereas the effect of methamphetamine was slightly attenuated. These results suggest that methamphetamine as well as tyramine and cocaine indirectly activates presynaptic alpha-2 adrenoceptors via norepinephrine released from adrenergic nerves to inhibit the twitch response. It is also suggested that the inhibitory effects of methamphetamine and tyramine may be partially mediated by direct activation of presynaptic alpha-2 adrenoceptors by themselves.View full abstractDownload PDF (383K) -
Taeko HATA, Yoshitaka NISHIMURA, Tomitaro KITA, Atsufumi KAWABATA, Eij ...1987 Volume 45 Issue 3 Pages 365-372
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe electrocorticogram (ECoG) in a SART (specific alternation of rhythm in temperature)-stressed (repeatedly cold-stressed) rat, which is regarded as an experimental model for clinical vagotonic-type dysautonomia, was investigated in the present study by the power spectral technique. 1) Analysis of ECoG in SARI-stressed rats during the resting-arousal state indicated a decrease in total power and a decrease in relative power in the δ band, and also an increase in relative power in the θ, α and β bands. 2) In the slow-wave sleeping state, the ECoG of SARI-stressed rats indicated a marked increase in total power, an increase in the δ band and decreases in θ, α and β bands. 3) Electric stimulation of the posterior-hypothalamic area evoked alterations of ECoG similar to those caused by SART stress. ECoG response to electric stimulation in SART-stressed rats was less than that in unstressed rats. 4) Lesioning of the posterior-hypothalamic areas prevented SART stress-induced ECoG alterations. SARI-stressed rats thus appear to be at a higher consciousness level on awakening but to sleep more soundly. They seem to exhibit greater fluctuation in brain activity than normal rats. There is also the possibility that the posterior-hypothalamic area is responsible to some degree for ECoG alterations in SART-stressed rats.View full abstractDownload PDF (422K) -
Masayoshi GOTO, Nobutaka DEMURA, Takashi SAKAGUCHI1987 Volume 45 Issue 3 Pages 373-378
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of a newly synthesized xanthine derivative propentofylline (3, 7-dihydro-3-methyl-1-(5-oxohexyl)-7-propyl-1H-purine-2, 6-dione) on learning and memory of rodents were examined in the two different paradigms. In a shuttle box active avoidance paradigm, propentofylline (25 mg/kg/day, p.o.) improved the decreased learning ability of 12-month-old spontaneously hypertensive rats. Normotensive Wistar-Kyoto rats at a comparable age showed rapid acquisition of avoidance learning, which was not influenced by propentofylline. Step-down passive avoidance task was carried out as the other paradigm. The protein synthesis inhibitor cycloheximide (CXM) induced amnesia in young adult mice. Propentofylline improved the memory deficit when intraperitoneally administered 30 min before the retention test, and it also prevented the development of amnesia when injected 15 min before CXM. These results suggest that propentofylline ameliorates the disturbed learning and memory.View full abstractDownload PDF (298K) -
Takashi SHIGA, Mikio NAKAZAWA, Shoichi IMAI1987 Volume 45 Issue 3 Pages 379-387
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSUsing the product of heart rate (HR) and left ventricular developed pressure (LVP) as a measure of the total mechanical energy required for contraction (TMEFC), experiments were performed with isolated perfused heart preparations of the guinea pig to establish the importance of TMEFC before induction of ischemia for induction of calcium accumulation within ischemic reperfused myocardium. Two calcium antagonists, diltiazem and nicardipine, and prazosin produced a doserelated suppression of the calcium accumulation when given prior to induction of ischemia (except for the highest dose of nicardipine), while they were ineffective when given only during the period of reperfusion, and the suppression was found to be closely correlated with the decrease in HR×LVP before induction of ischemia. The failure of the highest dose of nicardipine to suppress calcium accumulation (while producing a dose-related decrease in HR×LVP) was not associated with an increase in cyclic AMP. These findings are compatible with the idea that TMEFC before induction of ischemia is a prime determinant of calcium accumulation within the ischemic reperfused myocardium.View full abstractDownload PDF (482K) -
Keiji KOMORIYA, Ikuo NAGATA, Keiko KUNISAWA, Toru TAKESHITA, Tatsuyuki ...1987 Volume 45 Issue 3 Pages 389-396
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSTI-31 (TEI-3096, 6-p-chlorobenzyl-5H-2, 3, 6, 7-tetrahydro-5, 7-dioxothiazolo[3, 2-a]pyrimidine) reduced bovine type II collagen-induced arthritis (CIA) in rats in a time and dose-dependent manner. Oral TI-31 treatment in doses of 10 and 50 mg/kg daily for 7 days prior to collagen immunization depressed the development of arthritis. However, it had no obvious effect on CIA when administered daily for a 7-day or 28-day period after the immunization. This compound was also ineffective against the established arthritis. On the contrary, cyclophosphamide, dexamethasone, or ibuprofen strongly protected the animals from the development of arthritis and/or cured the established arthritis by these dose regimens. Both humoral and delayed-type hypersensitivity skin responses to bovine type II collagen were decreased in rats treated with TI-31 daily for 7 days before the induction of arthritis. These results suggest that TI-31 depresses CIA by regulating the immune response to collagen through a mechanism different from that of anti-inflammatory drugs or immunosuppressants.View full abstractDownload PDF (379K) -
Yasuhiro OHBA, Yasuyuki SHIRAKI, Kazushige SAKAI1987 Volume 45 Issue 3 Pages 397-404
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe vasorelaxing effects of nicorandil (NCR), isosorbide dinitrate (ISDN) and nitroglycerin (NTG) were studied in isolated canine coronary arteries. In rings of coronary arteries precontracted with prostaglandin F2α (3×10-6 M) or KCI (30 mM), removal of the endothelium significantly augmented the relaxing effects of NCR, while it did not affect those of ISDN and NTG. In unrubbed rings precontracted with KCI (30 mM), methylene blue (5×10-6 M) significantly inhibited vasorelaxing responses to the three drugs. The order of the inhibition was as follows: NTG>ISDN>NCR. When the unrubbed tissue was incubated with NTG (10-5 M) or ISDN (10-4 M) for 10 min, it developed acute tolerance in relaxing response to NTG or ISDN. Unlike NTG and ISDN, NCR did not develop any tolerance. The treatment with N-acetylcysteine (5×10-5 M) tended to potentiate relaxant effects of NTG and to reduce the degree of acute tolerance to NTG. The results suggest that cGMP plays a role in the relaxation of the coronary artery induced by the drugs and furthermore that the mode of the vasorelaxing action of NCR may be somewhat different from that of NTG or ISDN.View full abstractDownload PDF (478K) -
Tomochika OHNO, Nakako HIROSE, Hiroshi URAMOTO, Takafumi ISHIHARA, Sus ...1987 Volume 45 Issue 3 Pages 405-415
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe time-course of gastric mucosal surface epithelial cell damage and macroscopically visible lesions in response to restraint and water-immersion stress (22°C) in rats was examined, and the effects on it of 16, 16-dimethyl prostaglandin E2 (dmPGE2) were compared with those of papaverine, timoprazole and atropine. The stress produced surface epithelial cell damage prior to visible lesion, the former increasing in severity with time and reaching a plateau 60 min later, by which time exfoliation of surface epithelial cells was observable along the mucosal folds. In contrast, macroscopically visible lesions appeared 2 hr after stress, and severity continued to increase with time. Pretreatment injections (s.c.) of dmPGE2 (3, 30 μg/kg), papaverine (100 mg/kg) and atropine (1 mg/kg) protected the surface cells against stress (1 hr)-induced damage, and inhibited visible lesion formation after 4 hr stress. Timoprazole (30 mg/kg, s.c.) did not protect the surface cells, but did markedly inhibit visible lesion formation. dmPGE2, papaverine and atropine, but not timoprazole, inhibited stress-induced increases in gastric contractions. dmPGE2, timoprazole and atropine, but not papaverine, inhibited acid secretion in stress-conditions. These results indicated that stress induced damage to the gastric mucosa within 1 hr due to increased gastric contractions, and the surface epithelial cell damage developed into macroscopically visible lesions in the presence of acid, and that dmPGE2 protected the surface epithelium against stress-induced damage probably by inhibiting gastric contractions.View full abstractDownload PDF (678K) -
Effect of Tritoqualine on the Proliferation of Interleukin-3 Dependent Cell Line and Sensitive CellsYoshio NAKAGAWA, Tomoko OGAWA, Kohei UMEZU, Shigeru SATO1987 Volume 45 Issue 3 Pages 417-424
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn this paper, the effect of tritoqualine (TRQ) on the proliferation of interleukin (IL) sensitive cells was investigated. TRQ inhibited the proliferation of FDCp-2 (IL-3 dependent cell line), CTLL-2 (IL-2 dependent cell line) and bone marrow cells (BMC) stimulated by IL, giving an ID50 of about 3 μM equally in the three systems. However, a ten times higher concentration of TRQ was required to inhibit the tumor cell proliferation. TRQ did not affect the unstimulated bone marrow cells. Accordingly, it is suggested that TRQ may show its anti-allergic effect, at least partially, by interfering with the proliferation/differentiation to mast cell and basophils of multi-functional hemato-poietic cells stimulated by IL-3.View full abstractDownload PDF (347K) -
Phorbol Ester Potentiates α1-Adrenoceptor-Mediated Positive Inotropic Effect in Rat Papillary MuscleHitomi OTANI, Hajime OTANI, Dipak K. DAS1987 Volume 45 Issue 3 Pages 425-428
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSTumor-promoting phorbol esters may alter α1-adrenoceptor-mediated cardiac response by stimulating protein kinase C activity. We investigated the effect of phorbol-12, 13-dibutyrate (PDBu) on the positive inotropic effect (PIE) in rat left ventricular papillary muscle. PDBu (1-100 nM) potentiated the phenylephrine (PE)-induced PIE in a dose and time-dependent manner. The PIE induced by PE and PDBu was abolished by pretreatment with 3×10-7 M prazosin. PDBu also enhanced PE-induced slow responses 2- to 3-fold. These results suggest that PDBu enhances α1-adrenoceptor mediated PIE by potentiating slow Ca2+ channels, presumably through the activation of protein kinase C.View full abstractDownload PDF (181K) -
Hiroshi OZAKI, Koichi SATO, Takumi SATOH, Hideaki KARAKI1987 Volume 45 Issue 3 Pages 429-433
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn rat aortic strips loaded with a Ca2+ indicator, fura 2, the Ca2+ signal and contractile tension were simultaneously recorded. On the addition of high K+ or noradrenaline, the 500 nm fluorescence produced by excitation at 340 nm increased and that produced by excitation at 380 nm decreased. EGTA decreased the 340 nm fluorescence and increased the 380 nm fluorescence in resting and stimulated muscles. Tension changes were always preceded by fluorescent changes.View full abstractDownload PDF (240K) -
Tadayoshi TAKEUCHI, Osamu YAGASAKI1987 Volume 45 Issue 3 Pages 434-437
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of arachidonic acid and mepacrine on ACh release from guinea-pig ileum myenteric plexus were investigated. Mepacrine (1-8 μM) inhibited the ACh release in a concentration-dependent manner. Arachidonic acid counteracted the inhibitory effect of mepacrine, but PGE2 did not. The inhibition induced by a combination of mepacrine and indomethacin on nicotine-induced ACh release was prevented by arachidonic acid, while that on spontaneous ACh release was prevented by arachidonic acid and PGE2 added simultaneously. The roles of arachidonic acid and PGs in the ACh release will be discussed.View full abstractDownload PDF (241K)
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