巻号一覧
42 巻 (1986)
- 4 号 p. 457-
- 3 号 p. 333-
- 2 号 p. 153-
- 1 号 p. 1-
42 巻, 4 号
選択された号の論文の19件中1～19を表示しています
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Yukio UMEDA, Keiji NAKAMURA1986 年 42 巻 4 号 p. 457-463
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーChronic gastric ulcers were produced by injection of 20% acetic acid (0.05 ml) into the submucosal layer of the rat stomach in order to determine the effects of the prostanoid trimoprostil on the healing and recurrence of ulcers. Local injection of acetic acid solution produced large demarcated ulcers in all animals on day 5, which rapidly decreased to reach low levels on days 40-80 and then became exacerbated on day 100. The exacerbation of the ulcer is probably recurrence. Trimoprostil was administered ad libitum in drinking water containing 0.1, 0.3 and 1.0 μg/ml (average dose 12.4, 37 and 124 μg/kg/day) for a period of 14 days (day 1-15) to assess its effect on healing and for a period of 40 days (day 60-100) to assess its ability to prevent recurrence. The higher two doses of trimoprostil accelerated the spontaneous healing of the ulcers. Furthermore, trimoprostil, at both doses, prevented the observed recurrence of this type of ulcer. Trimoprostil dose-dependently (30-300 μg/kg, p.o.) inhibited gastric secretion in pylorusligated rats. Cimetidine at the antisecretory dose (1 mg/ml, 132 mg/kg/day) failed to affect the healing process of gastric ulcers, but tended to prevent the recurrence of gastric ulcers. Our present study suggests that trimoprostil is a promising antiulcer drug for the treatment of chronic gastric ulcer.抄録全体を表示PDF形式でダウンロード (333K) -
Yoshio SUZUKI, Mikio ITO, Naoto SAITO1986 年 42 巻 4 号 p. 465-475
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーThe present study was made to clarify the mechanisms of the antinephritic action of SA-446, an angiotensin I converting enzyme inhibitor, on crescentic-type anti-GBM nephritis in rats as compared to the actions of spironolactone (an antialdosterone agent), kallidinogenase (a kallikrein agent) and saralasin (an angiotensin II antagonist). SA-446 (25 mg/kg/day, p.o.) had a tendency to reduce the urinary protein excretion and plasma urea nitrogen content. In addition, this drug remarkably inhibited not only glomerular histopathological changes (i.e., crescent formation, the adhesion of capillary walls to Bowman's capsule and fibrinoid necrosis) but also the elevation of blood pressure. Spironolactone (25 mg/kg/day, p.o.) and kallidinogenase (25 KU/day, Lm.) also showed beneficial effects on glomerular histopathological changes and hypertension, although both drugs were not as effective as SA-446. However, saralasin (72 μg/day, s.c.) caused a marked aggravating action on this nephritis. This nephritic model showed a marked low activity of plasma renin all through the 40 day experimental period. In this model, the urinary aldosterone excretion was increased, in spite of the decrease in plasma renin activity. SA-446 and kallidinogenase significantly inhibited the decrease in plasma renin activity and the increase in urinary aldosterone excretion. Spironolactone inhibited only the increase in the aldosterone excretion. However, saralasin decreased the plasma renin activity under the control level and strongly increased the urinary aldosterone excretion (about 1.8 times the control level on the 20th day). These results suggest that the antinephritic effect of SA-446 may be related to the anti hypertensive action and the increase in renal blood flow through activation of the kallikrein-kinin and prostaglandins systems.抄録全体を表示PDF形式でダウンロード (671K) -
Yukio KISHI, Fujio NUMANO1986 年 42 巻 4 号 p. 477-485
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーWe investigated the effect of amrinone, a non-glycosidic, non-adrenergic cardiotonic drug, on rabbit aortic strips and vascular smooth muscle cells cultured from rabbit aorta. Amrinone relaxed the strips precontracted by KCl, norepinephrine, serotonin or STA2 in a dose-dependent manner, and it shifted the dose-response curves downward. A similar mode of relaxation was noted with IBMX, an inhibitor of cyclic AMP phosphodiesterase (cAMPPDE). Although propranolol did not affect the relaxation induced by amrinone, W-7, a calmodulin antagonist, slightly potentiated and IBMX attenuated the response. In intact smooth muscle cells in culture, amrinone increased basal levels of cAMP and markedly potentiated cAMP accumulation in response to 10-6 M isoproterenol. The effect on cAMP accumulation mimicked that of IBMX but the effects were not additive. Inhibition of cAMPPDE was also demonstrated in a cell-free system, IC50 values for amrinone and IBMX being 2.1×10-5 M and 1.2×10-6 M, respectively, using a preparation of cAMPPDE partially purified from the cells by DEAE cellulose chromatography. Amrinone seems to exert a direct effect on vascular smooth muscle cells by potently inhibiting cAMPPDE. This inhibition would to some extent explain the vasodilatory property.抄録全体を表示PDF形式でダウンロード (454K) -
Norihisa INAZU, Hiroshi KOGO, Tetsuo SATOH1986 年 42 巻 4 号 p. 487-491
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーThe effects of clomiphene citrate (clomiphene) on the in vitro conversion of 13, 14-dihydro-15-keto-prostaglandin F2α (15KD-PGF2α) to 13, 14-dihydro-prostagland in F2α (13, 14H22-PGF2α) in the presence of rat ovarian homogenate, and the relationship between clomiphene and gonadotropin or estrogen in the conversion were investigated. Although clomiphene inhibited the increased conversion of 15KD-PGF2α 13, 14H2-PGF2α by pregnant mare serum gonadotropin (PMS) in rat ovary, the drug did not inhibit the decreased conversion of 15KD-PGF2α by estradiol. The 3-day administration of clomiphene reduced the conversion of 15KD-PGF2α to13, 14H2-PGF2αdose-dependently. A single administration of clomiphene also decreased the conversion, and this decreasing effect was similar to that of estradiol. On the other hand, the repeated administration of clomiphene decreased the ovarian and uterine weights and also inhibited the increase of the uterine weight by PMS or estradiol. These results suggest that clomiphene affects the ovarian enzyme catalyzing the conversion of 15KD-PGF2α to 13, 14H2-PGF2α.抄録全体を表示PDF形式でダウンロード (304K) -
Junichiro AONO, Kazushige SAKAI1986 年 42 巻 4 号 p. 493-500
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーThe present study was designed to examine the antiplatelet activity of SGB-1534, 3-[2-[4-(o-methoxyphenyl)-1-piperazinyl]ethyl] -2, 4(1H, 3H)-quinazolinedione monohydrochloride, compared with prazosin, ketanserin and aspirin. The equihypotensive doses of SGB-1534, prazosin and ketanserin were administered orally to rats; and 1 hr later, their effects on collagen-induced platelet aggregation, compared with those of aspirin, were examined under ex vivo conditions. The bleeding time was determined by using the tail transection method. SGB-1534 (10 mg/kg) as well as ketanserin (3 and 10 mg/kg) and aspirin (10 mg/kg) effectively inhibited the platelet aggregation; and in addition, they significantly prolonged bleeding times. Prazosin in doses of 10 and 30 mg/kg did not affect either the aggregation or bleeding times. Whereas 10-4M aspirin significantly inhibited the production of malondialdehyde (MDA) in rat platelets, SGB-1534, prazosin and ketanserin even in considerably high concentrations (10-4 or 10-3 M) did not affect the MDA production and the cyclic AMP levels in the platelets. In isolated rat femoral arteries, SGB-1534, prazosin and ketanserin antagonized the contractile response to phenylephrine with pA2 values of approximately 10.06, 10.39 and 7.71, respectively. Also, SGB-1534 and ketanserin attenuated the contractile response to 5-hydroxytryptamine (5-HT) with pA2 values of 6.36 and 9.53, respectively, while prazosin had no antagonistic effects on 5-HT-induced contraction.抄録全体を表示PDF形式でダウンロード (448K) -
Kazuhiko KUBOTA, Masahiro ITONAGA1986 年 42 巻 4 号 p. 501-506
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーTwo β-carbolines, methyl β-carboline-3-carboxylate (β-CCM) and ethyl β-carboline-3-carboxylate (β-CCE), caused the parallel shift of the doseresponse curve for cholecystokinin (CCK) in isolated guinea-pig gallbladder muscle. The Schild plot regarding the parallel shift in the dose-response curves had a regression line with a slope of 1.03 and a pA2 value of 5.17 for β-CCE, while the method of van Rossum gave a pA2 value of 5.24 for β-CCE and 5.53 for β-CCM. Both the β-carbolines protected CCK receptors in the gallbladder muscle from alkylation by dibenamine, but β-CCM did not protect acetylcholine receptors from dibenamine alkylation. These results suggest that 9-CCM and 3-CCE, so-called inverse agonists of benzodiazepines (BZP), antagonize the CCK action in the gallbladder muscle in a competitive manner, and the antagonism takes place at CCK receptor sites. No spare receptors for CCK were found in the guinea-pig gallbladder muscle.抄録全体を表示PDF形式でダウンロード (348K) -
Hiromi TSUSHIMA, Mayumi MORI, Tomohiro MATSUDA1986 年 42 巻 4 号 p. 507-515
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーEffects of methionine-enkephalin (ME) and 2-D-alanine-5-methionineenkephalinamide (DAMEA) microinjected into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, which contain neurons synthesizing and releasing antidiuretic hormone, upon the outflow and the osmotic pressure of urine and the other visceral functions were studied in a rat which was loaded with water and anesthetized with ethanol. These opioid peptides when microinjected into the SON or PVN induced potent antidiuretic effects in dose-dependent and timedependent manners with no significant effects on the other visceral functions. The approx. ED50 values for DAMEA were 1.3 (in the SON) and 0.7 (in the PVN) nmol, and the values for ME were 110 (in the SON) and 60 (in the PVN) nmol. The antidiuretic effects showed slow onset and long duration, with a minimal urine outflow at approx. 0.5 hr after microinjection and an approx. 2 hr-duration. The effects induced by the opioid peptides were inhibited by pretreatment with naloxone or atropine, without effects of pretreatment with alpha or beta-adrenoceptor antagonists, suggesting that the antidiuretic effects were mediated through an opioid receptor having low sensitivity to naloxone and also possibly mediated through a muscarinic receptor which was stimulated probably by the ACh released by the opioid peptides.抄録全体を表示PDF形式でダウンロード (531K) -
Kazuichi NATORI, Yuko OKAZAKI, Takeshi NAKAJIMA, Toshiyuki HIROHASHI, ...1986 年 42 巻 4 号 p. 517-523
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーIn order to elucidate the mechanism of action of DL-melinamide [DL-MA, N-(α-methylbenzyl)linoleamide], an inhibitor of cholesterol absorption, the effect of DL-MA on esterification of cholesterol in the mucosa of rabbit small intestine was studied. DL-MA inhibited acyl CoA:cholesterol acyltransferase (ACAT, EC 2.3.1.26) activity in the mucosal microsomes, with 50% inhibition occurring at approximately 0.5 μM. On the other hand, DL-MA had no effect on the cholesterol esterase (EC 3.1.1.13) activity in the mucosal cytosol. Kinetic studies indicate that DL-MA is an uncompetitive inhibitor of ACAT. D-MA, one of the two optical isomers of DL-MA, was found to be a more effective inhibitor of ACAT than L-MA, another isomer. This finding indicates that the inhibition of cholesterol absorption by DL-MA depends on the inhibition of ACAT by this compound, in view of the fact that D-MA is a more effective inhibitor of cholesterol absorption than L-MA.抄録全体を表示PDF形式でダウンロード (401K) -
Yoshimi NIWANO, Shigeo KONAKA, Matazaemon UCHIDA, Tatsuyoshi SUGIMOTO1986 年 42 巻 4 号 p. 525-529
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーMalotilate was orally administered to rats at a dose of 100 mg/kg 2 hr after partial hepatectomy. Mitochondrial state 3 respiration of the liver increased significantly from 23.4 nmol/min/mg protein in the control rats to 29.3 nmol/min/ mg protein in the rats administered with malotilate at 3 hr after the hepatectomy (1 hr after the administration). The administration also resulted in higher tendencies in the respiratory control ratio after 3, 6 or 20 hr (1, 4 or 18 hr after the administration) than in the control rats. Although partial hepatectomy made hepatic ATP concentration remarkably low, it gradually increased (from 1.53 μmol/g liver after 3 hr) to a level of 2.03 μmol/g liver after 20 hr in the rats administered with malotilate. No increase in ATP concentration was observed in the control rats. Correspondingly, the adenylate energy charge also showed higher tendencies in the malotilate administered rats. From these result, it is supposed that malotilate activates the mitochondria) functions which results in the increases of ATP concentration and adenylate energy charge. These changes in energy metabolism can be associated with accelerated regeneration of the liver by malotilate.抄録全体を表示PDF形式でダウンロード (227K) -
Junzo KAMEI, Tomokazu HOSOKAWA, Saizo YANAURA, Takehiko HUKUHARA1986 年 42 巻 4 号 p. 531-538
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーTo determine the role of central serotonergic systems in modulating the cough reflex, the effects of serotonergic agonists on the respiration and the cough reflex were comparatively studied. Male and female cats were anesthetized with sodium pentobarbital. Respiration and cough reflex were measured using a pneumotachograph via a cannula inserted into the trachea. The cough reflex was elicited by electrical stimuli to the superior laryngeal nerve. Tranylcypromine, a MAO inhibitor, in a dose of 5 mg/kg, i.v., increased the respiration, but depressed the cough reflex. The serotonin precursor 5-hydroxytryptophan (5 mg/kg, i.v.) depressed the respiration and the cough reflex. Haloperidol (2 mg/kg, i.v.) abolished the tranylcypromine-stimulated respiratory responses, and it intensified the tranylcypromine induced cough depression. It is concluded that the increase in serotonin levels in the brain has a depressant influence on the central generating mechanisms of the cough reflex. Furthermore, central dopaminergic mechanisms seem to play a modulating role on the cough reflex.抄録全体を表示PDF形式でダウンロード (384K) -
Hironori TANAKA, Shigeru UEKI, Koji TAKEUCHI, Susumu OKABE1986 年 42 巻 4 号 p. 539-548
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーEffects of indomethacin and cysteamine on the duodenal mucosa of rats were studied microscopically (using scanning electron microscopy) and also functionally. Indomethacin (5 mg/kg, s.c.) induced no microscopic damage to the duodenal epithelium for up to 6 hr after administration. Indomethacin had no effects on gastric H+ output and the amount of H+ in the duodenum, but did reduce the duodenal HCO3- secretion (both basal and 10 mM-HCl stimulated). PGE2 contents in the duodenal mucosa were markedly reduced by indomethacin for 6 hr. These results suggest that reductions of duodenal HCO3- secretion and endogenous prostaglandins per se do not impair the H+ disposal system of the duodenum and so do not damage the epithelial cells. In contrast, cysteamine (100 mg/kg, s.c.) produced microscopic damage to the duodenal epithelium as early as 2 hr later. Cysteamine significantly increased gastric H+ output and reduced duodenal HCO3-secretion, resulting in an increased amount of H+ in the duodenum 3 hr later. Cysteamine had no effect on PGE2 contents in the duodenum. The time lag between damage formation and functional changes suggests that the earliest damage caused by cysteamine occurs by mechanisms other than erosive action of H+ emptied by the stomach. The increased amount of H+ may contribute to an enhancement of the initial damage.抄録全体を表示PDF形式でダウンロード (682K) -
Koji TAKEUCHI, Hisashi YAMAKUNI, Youichi NOBUHARA, Susumu OKABE1986 年 42 巻 4 号 p. 549-560
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーWe examined the effects of 1 M NaCl as a mild irritant on gastric potential difference (PD), acid secretion, mucosal blood flow (MBF), and DNA synthetic activity in anesthetized rat stomachs and compared these effects with those of 4 M NaCl as a strong irritant. Both 1 M and 4 M NaCl produced a PD reduction (mucosal injury), but the reduced PD recovered faster in the mucosa exposed to 1 M NaCl as compared to 4 M NaCl. Acid secretion ceased after exposure to these hypertonic NaCl solutions, but histamine infusion (8 mg/kg/hr) stimulated acid secretion only in the mucosa exposed to 1 M NaCl. The MBF was significantly increased in response to 1 M NaClI, while exposure to 4 M NaCl had no effect on the MBF. These changes in acid secretion and MBF induced by 1 M NaCl were significantly antagonized by pretreatment with indomethacin (5 mg/kg, s.c.). The levels of PGE2 and 6-keto PGF1α in the corpus mucosa were significantly increased in the stomach exposed to both 1 M and 4 M NaCl, and these increases disappeared in the presence of indomethacin. The rate of [3H]-thymidine incorporation was significantly reduced in the mucosa after exposure to 4 M NaCl, but remained unaltered in the stomach exposed to 1 M NaCl. These results suggest that although both 1 M and 4 M NaCl produced mucosal injury (PD reduction) and enhanced PGs formation, a variety of functional alterations mediated by PGs occurred in response to injury in the stomach exposed to 1 M NaCl. The presence or absence of these functional responses may be associated with the biphasic actions on the gastric mucosa of these hypertonic NaCl solutions as mild and strong irritants.抄録全体を表示PDF形式でダウンロード (691K) -
Hiromu KAWASAKI, Koichiro TAKASAKI1986 年 42 巻 4 号 p. 561-570
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーThe role of presynaptic α-adrenoceptors in modulation of the 5hydroxytryptamine (5-HT) release from vascular adrenergic nerves was investigated in the perfused mesenteric vascular bed of the rat. After treatment with 5-HT (10 μM) for 15 min, the vasoconstrictor response to periarterial nerve stimulation (PNS, 4 to 16 Hz, 2 msec in duration for 30 sec) was greatly potentiated without significantly affecting the pressor response to exogenously administered noradrenaline (0.5 nmol). The potentiating effect was more pronounced at low frequencies of PNS (4 and 8 Hz), The potentiation of the pressor response to PNS after 5-HT treatment did not occur in the presence of LY53857 (0.01 μM), a selective 5-HT2 receptor antagonist. The enhanced pressor response to PNS seen after 5-HT treatment was further exaggerated in the presence of clonidine (0.1 and 1 μM), a preferential α2-adrenoceptor agonist, while methoxamine (1 and 10 μM), a selective α2-adrenoceptor agonist, did not affect the enhanced PNS response. This effect of clonidine was more pronounced in low frequencies of PNS (4 and 8 Hz) and was abolished by LY53857 (0.01 μM). In the perfused mesenteric vascular bed labelled with [3H]-5-HT, PNS (8 Hz) evoked an increase of tritium efflux in the perfusate. The PNS-evoked tritium efflux was facilitated by yohimbine (0.1 to 1 μM), an α2-adrenoceptor antagonist, and prazosin, a selective α1adrenoceptor antagonist, at a high concentration (1 μM), while LY53857 (0.01 to 0.1 μM) and a low concentration of prazosin (0.1 μM) had no effect on the tritium efflux. Clonidine (0.01 to 1 μM) produced a dose-dependent increase of PNS-evoked tritium efflux, while methoxamine (0.1 to 10 μM) was without effect. The monoamine uptake inhibitor, cocaine (10 μM) produced a significant inhibition of the PNS-evoked tritium efflux. The effects of clonidine and cocaine on the PNS-evoked tritium efflux were antagonized by yohimbine (1 μM). These results suggest that the release of 5-HT from adrenergic nerve endings by PNS is modulated by presynaptic 2-adrenoceptors.抄録全体を表示PDF形式でダウンロード (540K) -
Tadahiro SHIKIMI, Masanori HANDA1986 年 42 巻 4 号 p. 571-574
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーEffects of human urinary trypsin inhibitor, urinastatin, a compound clinically prescribed for treatment of acute pancreatitis, on lysosomal thiol proteinases were studied. Urinastatin had inhibitory effect on the activities of cathepsins B and H in vitro. In the experimental acute pancreatitis induced by a closed duodenal loop, urinastatin prevented the enhancement of esterolytic activity and the activities of cathepsins B and H. Urinastatin also improved the activities of inhibitors of cathepsins B and H in the case of pancreatitis.抄録全体を表示PDF形式でダウンロード (180K) -
Junichiro AONO, Hiroyuki NABATA, Kazushige SAKAI1986 年 42 巻 4 号 p. 575-578
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーThe antiplatelet effect of fenflumizole, compared with aspirin or ticlopidine, was examined in in vitro, ex vivo and in vivo situations of the rabbit. Unlike ticlopidine, fenflumizole and aspirin effectively inhibited in vitro the platelet aggregation elicited by arachidonate and collagen. The activity of fenflumizole was 350 times more potent than that of aspirin. Fenflumizole (0.3-3 mg/kg) given p.o. was 4.2 and 8.1 times more potent than aspirin in inhibiting arachidonate and collagen-induced platelet aggregations, respectively. Ticlopidine (300 mg/kg, p.o.) resulted in only weak effects on the aggregations. Fenflumizole (3 mg/kg) as well as aspirin (10 mg/kg) given p.o., unlike ticlopidine (300 mg/kg), effectively prevented the arachidonate-induced sudden death.抄録全体を表示PDF形式でダウンロード (208K) -
Issei TAKAYANAGI, Fukio KONNO, Hiroyuki KAMEDA, Haruichi KUBO, Akira F ...1986 年 42 巻 4 号 p. 579-582
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーOptical isomers of YM-12617, a potent and selective alpha1 -adrenoceptor blocker, were tested on the rabbit iris dilator and aorta. The order of potency was R(-)- isomer>racemate>S(+)-isomer. The R(-)-isomer and racemate behaved as an essentially irreversible antagonist to norepinephrine in the iris dilator where the efficacy of norepinephrine was small, although the S(+)-isomer was a competitive antagonist. These drugs behaved as a competitive antagonist of norepinephrine in the aorta where the efficacy of norepinephrine was large.抄録全体を表示PDF形式でダウンロード (221K) -
Toru EGASHIRA, Ritsuko TAKANO, Yasumitsu YAMANAKA1986 年 42 巻 4 号 p. 583-586
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーCerebrospinal fluid (CSF) from dogs competitively inhibited A-form MAO, but was non-competitive with B-form MAO. Heat treatment of CSF (90°C, 20 min) had no effect on the inhibition. Digestion with trypsin and chymotrypsin reduced the MAO inhibitory activity. After ultrafiltration of the CSF through a membrane to remove substances of >5, 000 M.W., significant inhibitory activity persisted. These results suggest that CSF contains endogenous substances that act like MAO inhibitor to inhibit A and B-form MAO, and these substances are peptides of less than 5, 000 M.W.抄録全体を表示PDF形式でダウンロード (184K) -
Takuo SATO, Yoshitaka INO, Yoshiko KOSHIYAMA, Akemi MOTOYOSHI, Minoru ...1986 年 42 巻 4 号 p. 587-589
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーFUT-175 inhibited the zymosan-induced rat paw edema in a dosedependent manner, while indomethacin exhibited no significant activities in this model. FUT-175 also inhibited the decrease in hemolytic complement (CH50) induced by zymosan in vitro, and indomethacin was inactive. These results suggest that FUT-175 has potent in vitro and in vivo inhibitory activity against the activation of the complement system induced by zymosan.抄録全体を表示PDF形式でダウンロード (149K) -
Takashi TANIGUCHI, Motohatsu FUJIWARA, Yoshinori MASUO, Ichiro KANAZAW ...1986 年 42 巻 4 号 p. 590-593
発行日: 1986年
公開日: 2006/09/15
ジャーナル フリーWe investigated the contents of neurokinin A, neurokinin B and substance P in the rabbit iris sphincter muscle, combining HPLC and radioimmunoassay, as our previous reports indicated that a slow component of neurogenic contractions of this muscle is most probably mediated by such tachykinins. The concentrations of these tachykinins were 44.3±8.7 fmol/mg protein, 35.3±10.2 fmol/mg protein and 186.8±29.8 fmol/mg protein (N=4), respectively. These results demonstrated that neurokinin A, neurokinin B and substance P are all present in the rabbit iris sphincter muscle.抄録全体を表示PDF形式でダウンロード (208K)
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