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Volume 62 (1993)
- Issue 4 Pages 331-
- Issue 3 Pages 215-
- Issue 2 Pages 123-
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Volume 62, Issue 1
Displaying 1-19 of 19 articles from this issue
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Masaomi Umeda, Kooichi Saida1993 Volume 62 Issue 1 Pages 1-7
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSWe examined the cardioprotective effect of nisoldipine against myocardial dysfunction during ischemia and reperfusion in comparison with those of diltiazem and nifedipine in rabbit hearts perfused at constant pressure. These calcium antagonists were administered to the hearts before 60 min of ischemia. They inhibited the increase of end-diastolic pressure during ischemia in a dose-dependent manner. Diltiazem at 1.0 μM, nifedipine at 3.0 μM and nisoldipine at 0.01 μM produced the maximal cardioprotec tive effect. Nisoldipine had a beneficial effect with less negative inotropic effect than those of diltiazem and nifedipine and it produced a significant increase of coronary flow during reperfusion. When the vascular component was eliminated under constant flow perfusion, nisoldipine also showed the cardioprotective effect. Nisoldipine did not produce any beneficial effect without the inhibition of the increase in end-diastolic pressure during ischemia nor did it do so without the increase of reperfusion flow. Therefore, the nisoldipine-increased coronary flow during reperfusion as well as the inhibition of ischemic contracture by nisoldipine seems to play a crucial role in improving the myocardial dysfunction of ischemic-reperfused hearts.View full abstractDownload PDF (433K) -
Yoko Aniya, Ai Daido1993 Volume 62 Issue 1 Pages 9-14
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSThe effect of t-butyl hydroperoxide (t-BuOOH), cumene hydroperoxide (CuOOH) or linoleic acid hydroperoxide (linoleic-OOH) on liver microsomal glutathione S-transferase of rats was studied in vitro. When microsomes were incubated with either 100 μM t-BuOOH or 25 μM CuOOH, glutathione S-transferase activity was increased 1.5-fold; activity was further increased to 2.2-fold in the presence of small amounts of glutathione. The same amounts of dithiothreitol or cysteine did not enhance the t-BuOOH or CuOOH-induced increase in transferase activity. The transferase activity was also increased 1.4-fold by 10 μM linoleic-OOH plus 1 M glutathione. The increase in microsomal glutathione S-transferase activity after treatment of microsomes with t-BuOOH in the presence of glutathione was completely reversed by addition of dithiothreitol, whereas the activation of the transferase caused by t-BuOOH in the absence of glutathione was not reversed. Although microsomal glutathione S-transferase also possesses glutathione peroxidase activity, only transferase activity was increased by t-BuOOH in either the presence or absence of glutathione. These data indicate that microsomal glutathione S-transferase is activated by organic hydroperoxides in either the absence or presence of small amounts of glutathione, suggesting an activation of the transferase by thiol oxidation of the cysteine residue.View full abstractDownload PDF (445K) -
Minoru Narita, Yuki Takahashi, Kazuaki Takamori, Masahiko Funada, Tsut ...1993 Volume 62 Issue 1 Pages 15-24
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSThe antinociception of intracerebroventricular injection (i.c.v.) of morphine was markedly abolished by pretreatment with naloxonazine (μ1-antagonist), s.c.; β-funaltrexamine (μ1/μ2-antagonist), i.c.v.; DSP-4 (noradrenaline neurotoxin), s.c.; or p-chlorophenylalanine (serotonin synthesis inhibitor), s.c. in the mouse 55°C hot-plate assay. Pretreatment with nor-binaltorphimine (κ-antagonist), i.c.v. or PCPA, s.c. drastically blocked the κ-agonist U-50, 48811-induced supraspinal antinociception. These findings in dicate either noradrenergic or serotonergic involvement in the mediation of the antinociception of i.c.v.-morphine through μ-receptors. On the contrary, the antinociception of i.c.v. U-50, 488H through κ-receptors appears to depend on the serotonergic but not noradrenergic systems. The antinociceptive interaction between the i.c.v.-morphine and -U-50, 488H was an additive effect. On the other hand, i.c.v.-morphine dose-dependently increased the locomotion in mice, and this hyperlocomotion of morphine was drastically blocked by pretreatment with either β-funaltrexamine, i.c.v. or 6-hydroxydopamine (dopamine depletor), i.c.v. I.c.v.-U-50, 488H dose-dependently reduced the increasing locomotion of i.c.v.-morphine, but not that of s.c.-apomorphine (dopamine receptor agonist), and this effect of U-50, 488H was completely reversed by pretreatment with nor-binaltorphimine, i.c.v. These results suggest that coadministration of κ-agonists can suppress the dopamine-related hyperlocomotion of μ-agonists without decreasing the antinociception of μ-agonists in mice.View full abstractDownload PDF (717K) -
Susumu Okabe, Keiko Takagi, Katsumoto Inoue1993 Volume 62 Issue 1 Pages 25-33
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSWe examined the effect of NC-1300-O-3 on the healing of acetic acid-induced gastric ulcers in male Donryu rats. NC-1300-O-3, administered orally once daily for 2, 4 or 8 weeks after ulceration, significantly accelerated the spontaneous healing of both fresh and unhealed ulcers (induced by pretreatment with indomethacin). The delay in ulcer healing caused by indomethacin was markedly prevented by concurrent administration of NC-1300-O-3 once daily for 4 weeks in a dose-related manner. A bolus administration of NC-1300-O-3 to rats with 5-day-old ulcers potently and persistently (>48 hr) inhibited both the basal and histamine-stimulated gastric secretion. However, the potency and duration of the antisecretory activity of the compound, with or without indomethacin, gradually decreased with the period of treatment. After an 8-week treatment with NC-1300-O-3 alone, the volume of the gastric contents was markedly increased, resulting in an increased acid output. Administration of the compound together with indomethacin for 8 weeks resulted in a significant increase in the volume, no change in acid output and a significant increase in the pH. The spontaneous or delayed healing of gastric ulcers induced 4 weeks after pretreatment with NC-1300-O-3 was also significantly enhanced or prevented with NC-1300-O-3, with a weakened antisecretory activity. Therefore, NC-1300-O-3 seems to promote ulcer healing or prevents delayed healing by its potential antisecretory and/or ulcer-healing activities.View full abstractDownload PDF (685K) -
Ikuko Kimura, Mari Okazaki, Masayasu Kimura1993 Volume 62 Issue 1 Pages 35-41
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSAcetylcholine (ACh) release from the motor nerve terminal in the streptozocin-induced diabetic state was studied in mouse phrenic nerve-diaphragm muscle preparations. Electrically evoked release of 3H-ACh from the preparation preloaded with 3H-choline was measured during two consecutive periods of stimulation (S1 and S2). In diabetic mice, the amount of 3H-ACh release during S2 was decreased, and the evoked ACh release declined more steeply with successive stimulation periods than in normal ddY mice. The decrease in release was restored when the presynaptic autoreceptors were stimulated by accumulating ACh under the irreversible inhibition of junctional cholinesterase by methanesulfonyl fluoride. This effect was abolished by the administration of (+)-tubocurarine (5 μM). In diabetic mice, the biphasic (acceleration and suppression) effect by succinylcholine on evoked ACh release was caused at 3- to 10-fold lower concentrations than in normal mice. The degree of enhancement of resting 3H-overflow by succinylcholine (10 and 30 μM) was greater in the diabetic state. These results indicated that in the diabetic state, the decrease in evoked ACh release interferes with its presynaptic action on inducing further release (positive feedback modulation) via the presynaptic nicotinic ACh receptor (n-AChR). The presynaptic hypersensitivity to succinylcholine may be due to the augmentation of presynaptic n-AChR sensitivity caused by the reduction of evoked ACh release in the diabetic state.View full abstractDownload PDF (489K) -
Kenji Honda, Yukio Takano, Hiro-o Kamiya1993 Volume 62 Issue 1 Pages 43-47
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSWe have examined the pharmacological subtypes of muscarinic receptors mediating phosphoinositide hydrolysis and contraction in the longitudinal smooth muscle of guinea pig ileum with the use of muscarinic antagonists. Carbachol increased the formation of 3H-inositol phosphates (IPs) in a dose-dependent manner in both ileal smooth muscle and the frontal cortex of rats. The rank order of muscarinic antagonists for inhibition of IP formation induced by carbachol was 4-DAMP = atropine > pirenzepine > AF-DX 116 in guinea pig Real smooth muscle. In ileal smooth muscle, the inhibition by the M1 antagonist pirenzepine was about 15 times less than that by atropine. However, in the rat frontal cortex, the inhibition by pirenzepine was only about 3 times less than that by atropine. The inhibitory effect of the M2 antagonist AF-DX 116 was weak in both ileal muscle and the frontal cortex. The M3 antagonist 4-DAMP strongly inhibited carbachol-induced IP formation in ileal smooth muscle. The rank order of muscarinic antagonists for inhibition of contraction induced by 10-7 M carbachol was atropine ≥ 4-DAMP > pirenzepine > AF-DX 116. These results suggest that both IP formation and the contractile response induced by muscarinic agonists are mediated through the muscarinic M3 subtype in guinea pig ileum.View full abstractDownload PDF (372K) -
Mayumi Mori, Hiromi Tsushima, Tomohiro Matsuda1993 Volume 62 Issue 1 Pages 49-56
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSABSTRACT-The effects of injection of substance P (SP) into the hypothalamic supraoptic vasopres-sinergic nucleus (SON) in water-loaded and ethanol-anesthetized rats were examined. Substance P and its analog [D-Pro2, D-Trp7, 9]SP induced marked decreases in urine outflow, with a ED50 value of approx. 0.4 and 0.9 nmol, respectively. The antidiuresis of SP was inhibited by a prior injection of [D-Arg1, D-Trp7, 9, Leu11]SP (spantide), an SP-receptor antagonist into the SON. After the injection of SP, urine osmotic pressure was increased by threefold, and the urine level of arginine-vasopressin (AVP) was elevated by 70-fold. The effects of SP and [D-Pro2, D-Trp7, 9]SP were completely blocked by pretreatment with an intravenous injection of d(CH2)5-D-Tyr(Et)VAVP, an AVP (V1V2)-receptor antagonist. A prior injection of atropine, a muscarinic receptor antagonist, inhibited the effect of [D-Pro2, D-Trp7, 9]SP, but not that of SP. The results suggest that SP, injected into the SON, causes antidiuresis through the release of AVP. A possible mechanism for the antidiureses induced by SP and [D-Pro2, D-Trp7, 9]SP is discussed.View full abstractDownload PDF (550K) -
Ryuji Takeda, Akira Haji1993 Volume 62 Issue 1 Pages 57-65
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSEffects of isoflurane on the membrane potential trajectory and synaptic activity in bulbar respiratory neurons were investigated in decerebrate, vagotomized and artificially ventilated cats. A 2-min inhalation of 1.6% end-tidal concentration of isoflurane produced depolarization of the membrane in 10 out of 18 inspiratory, 8 out of 15 post-inspiratory and 5 out of 12 expiratory neurons and hyperpolarization in the rest of the population recorded in the ventral respiratory group. In both depolarized and hyperpolarized cells, periodically occurring excitatory and inhibitory synaptic waves were decreased, and input resistance was increased. Concomitantly, isoflurane reduced the excitatory and inhibitory postsynaptic potentials evoked by electrical stimulation of the vagus nerve, superior laryngeal nerve and cervical spinal cord. The effects of isoflurane on membrane potential and input resistance became negligible when excitatory and inhibitory synaptic potentials were suppressed by iontophoretically applied tetrodotoxin. The present results suggest that the respiratory neuronal responses induced by isoflurane are attributed mainly to the decrease of excitatory and inhibitory synaptic interactions in the bulbar respiratory network of neurons.View full abstractDownload PDF (661K) -
Tokio Nakane, Kimiko Kawai, Shigetoshi Chiba1993 Volume 62 Issue 1 Pages 67-74
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSThe mechanism of pindolol-induced vasoconstriction in isolated and perfused dog coronary arteries was studied. Single injections of pindolol (1-100 μg), propranolol (1-30 μg), and 5-hydroxytryptamine (5-HT, 0.001-1 μg) produced a dose-related vasoconstriction in dog coronary arteries which were dilated by acetylcholine. l-Pindolol constricted coronary arteries, but d-pindolol did not. The responses to pindolol and propranolol were not affected by any of the following compounds (100 μg): bunazosin (a selective α1-adrenergic antagonist), DG 5128 (a selective α2-adrenergic antagonist), atropine (a muscarinic antagonist), chlorpheniramine (a selective H1-antagonist), cimetidine (a selective H2-antagonist), and ketanserin (a selective 5-HT2 antagonist). Methysergide (10 μg, a 5-HT1 and 5-HT2 antagonist) significantly reduced pindolol- and propranolol-induced vasoconstrictions, although it did not reduce norepinephrine-induced vasoconstriction in the presence of 5 μM propranolol. Methysergide (10 μg) and ketanserin (100 μg) significantly suppressed 5-HT-induced vasoconstriction. Diltiazem (100 μg, a calcium antagonist) and the incubation in Ca2+-free solution containing 1 mM EGTA for 1 hr significantly reduced the vasoconstrictions induced by pindolol and propranolol. The Ca 2+-free solution containing 1 mM EGTA abolished the vasoconstriction induced by 5-HT in the presence of 1 μM ketanserine. In a solution containing 20 mM KCl, the vasoconstrictions caused by pindolol and propranolol were enhanced in dog coronary arteries. These results indicate that the direct contractile effects of pindolol on dog coronary arteries are mediated, at least partly, through 5-HT1-like receptors, but not through α-adrenergic receptors. The vasoconstriction induced by pindolol appears to be associated with an increase of Ca2+ influx in the smooth muscle cell membrane.View full abstractDownload PDF (522K) -
Shigekatsu Kohno, Kohji Ogawa, Takeshi Nabe, Hideki Yamamura, Katsuya ...1993 Volume 62 Issue 1 Pages 75-79
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSWhether anaphylactic histamine release from rat peritoneal mast cells is influenced by betahistine, a histamine H1-receptor agonist/H3-antagonist, and dimaprit, an H2-agonist, was examined. Treatment with dimaprit at 6 and 60 μM for 20 min significantly inhibited the anaphylactic histamine release, whereas betahistine at up to 80 μM under the same conditions did not affect it. Treatment with dimaprit at 6 and 60 μM for 1 to 20 min and for 5 to 20 min, respectively, caused a time-dependent inhibition of the release, but up to 30 min treatment with 8 and 80 μM betahistine had no effect. The decreased histamine release induced by dimaprit was recovered by neither mepyramine nor cimetidine. However, thioperamide, an H3-selective antagonist, dose-dependently restored the diminished release. From these results, the inhibition of anaphylactic histamine release by dimaprit is not produced by the stimulation of H2-receptors, but involves the stimulation of H3-like receptors or H3-subtype receptors, which are distinct from the H3-receptors located in brain, and suggests that the receptor plays an important role in the negative feedback regulation of histamine release.View full abstractDownload PDF (378K) -
Satoshi Ono, Kazunori Kitamura, Mutsuko Maekawa, Kazunari Hirata, Moto ...1993 Volume 62 Issue 1 Pages 81-86
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSEffects of R(-)-1-(benzo[b]thiophen-5-yl)-2-[2-(N, N-diethylamino)ethoxy]ethanol hydrochloride (T-588) on normobaric hypoxia, histotoxic anoxia by KCN and complete ischemia by decapitation were investigated in mice. T-588 (30-100 mg/kg, p.o.) showed a significant and dose-dependent prolongation of the survival time in all of the models studied. Bifemelane (100-300 mg/kg, p.o.) was also protective against all the models. Tacrine was protective against hypoxia but had no effect on anoxia and ischemia. Imipramine was protective against anoxia, but shortened the survival time of hypoxic mice. It had no effect on ischemia. The anti-hypoxic effect of T-588 was completely inhibited by pretreatment with scopolamine (1 mg/kg, i.p.), while the anti-anoxic effect was partially inhibited. Its effect on the ischemia was not affected by scopolamine. Hypoxia decreased the cerebral contents of ATP, phosphocreatine and glucose and increased the contents of lactate in mice. T-588 had no effect on these changes. Bifemelane prolonged pentobarbital-induced sleeping time in mice with the doses inducing anti-anoxic action, but T-588 did not. These results suggest that the activation of the CNS cholinergic system is involved as one of the mechanisms for the anti-anoxic action of T-588.View full abstractDownload PDF (396K) -
Mitsuaki Sakashita, Kyomi Toyoda, Masaki Kitahara, Nobutomo Tsuruzoe, ...1993 Volume 62 Issue 1 Pages 87-91
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSABSTRACT-We studied the mechanisms of hypolipidemic effects of NIP-200 (3, 5-dimethyl-4, 6-diphenyl-tetrahydro-2H-1, 3, 5-thiadiazine-2-thione), a potent hypolipidemic compound, in cholesterol biosynthesis in the liver, cholesterol absorption in small intestine, and cholesterol catabolism and excretion in rats. NIP-200 did not reduce cholesterol biosynthesis and had no effects on cholesterol absorption in the small intestine. In the cholesterol catabolism and excretion, NIP-200 induced increases in cholesterol and bile acids levels in the bile and acidic steroids in the feces, and it enhanced cholesterol 7α-hydroxylase activity in the liver. These results suggest that NIP-200 increases the synthesis of bile acids as a result of the activation of cholesterol 7α-hydroxylase, the rate-limiting enzyme in the conversion of cholesterol to bile acids. Therefore, it is considered that one of the probable mechanisms of the serum total cholesterol lowering action of NIP-200 involves the enhancement of catabolism and excretion of cholesterol in the liver.View full abstractDownload PDF (359K) -
Norio Matsuki, Yuri Sakuma, Hiroshi Saito1993 Volume 62 Issue 1 Pages 93-97
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSBlood pressure and heart rate and responses to various physiological substances in suncus were characterized and compared with those in mice. The blood pressures of the two species were similar, but the heart rate of suncus (about 400 beat/min) was significantly lower than that of mice. Norepinephrine increased the blood pressure but decreased the heart rate in suncus. The latter was blocked by cervical vagotomy. Sensitivities to acetylcholine and isoproterenol were lower in suncus. These results suggest that regulation of blood pressure and heart rate in suncus is very unique and different from the well-defined system of the rodents.View full abstractDownload PDF (247K) -
Katsuro Shuto, Takashi Saito, Yoshihito Beppu, Yukiharu Ishida1993 Volume 62 Issue 1 Pages 99-102
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSEffects of OM-853 on behavioral responses in the forced swim test were studied. OM-853 significantly reduced the duration of immobility without any change in the exploratory activity. Imipramine also reduced the duration of immobility, but idebenone did not. On the other hand, vinpocetine enhanced the duration with a suppressive effect on ambulation. The anti-immobility effect of OM-853 was reversed by pretreatment with haloperidol. These results demonstrate that the effect of OM-853 on the swim test is different from that of idebenone and vinpocetine. Furthermore, the present results suggest that OM-853 may exert its anti-immobility activity through facilitated transmission of the dopaminergic and/or adrenergic systems.View full abstractDownload PDF (261K) -
Keiichi Enomoto, Kazuko Hayama, Masako Takano, Takeo Asakawa1993 Volume 62 Issue 1 Pages 103-106
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSAdenylate cyclase purified by affinity chromatography was activated about 2.5-fold in a Ca2+- and calmodulin-dependent fashion. G protein βγ-subunits, an inhibitor in the receptor-mediated inhibition of adenylate cyclase, inhibited the purified cyclase by more than 80%. The extent of βγ-induced inhibition was not affected by the activation with Ca2+ and calmodulin. Moreover, the prior addition of the βγ-subunits to the cyclase did not prevent the subsequent activation of the enzyme by Ca2+ and calmodulin. We conclude that the βγ-subunits inhibit adenylate cyclase activity in a calmodulin-independent mode.View full abstractDownload PDF (279K) -
Shinichi Nakamura, Yoshio Goshima, Jin-Liang Yue, Takeaki Miyamae, Yos ...1993 Volume 62 Issue 1 Pages 107-110
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSThe relevance of endogenously released DOPA to the (±)-nicotine-induced increase in locomotor activities was explored in rats. This increase was dose (0.1-1.0 mg/kg, s.c.)-dependent, stereo-selective and mecamylamine (1.0 mg/kg, s.c.)-sensitive, but was not antagonized by L-dopa methyl ester (200 pg, i.v.t.), a competitive L-dopa antagonist. Then, by microdialysis, low doses of α-methyl-p-tyrosine (α-MPT, i.p.) at 1-10 mg/kg, were tested to find a dose that selectively inhibits the basal DOPA release in the striata: the release was consistently inhibited by 3 mg/kg without any tendency to inhibit the basal dopamine release. Pretreatment with this dose did inhibit the nicotine-induced increases in locomotor activities. This suggests that endogenously released DOPA is in part relevant to the nicotine-induced behavior in rats.View full abstractDownload PDF (286K) -
Hisashi Kuribara, Yoshitaka Uchihashi1993 Volume 62 Issue 1 Pages 111-114
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSThe inhibitory actions of the selective dopamine D1 and D2-antagonists SCH 23390 and YM-09151-2, respectively, on the mouse''s discrete shuttle avoidance were almost equipotent at doses ranging from 0.01-0.1 mg/kg. SCH 23390 reduced the stimulant action of methamphetamine (0.5 mg/kg), MK-801 (0.1 mg/kg) and ketamine (10 mg/kg) with a similar potency. YM-09151-2 also antagonized the actions of these drugs, with the following order of effectiveness: ketamine > MK-801 > methamphetamine. The present results indicate that methamphetamine, MK-801 and ketamine have different characteristics of CNS stimulant action through dopamine D2-receptors.View full abstractDownload PDF (258K) -
Tadahiro Shikimi, Keisuke Hattori, Shuji Takaori1993 Volume 62 Issue 1 Pages 115-118
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSEffects of heparin on the inhibitory activities of human urinary trypsin inhibitor (ulinastatin) on trypsin, chymotrypsin and leukocyte elastase were studied. Heparin per se neither influenced the enzymatic activities nor changed the mode of inhibition of ulinastatin on the enzymes. In the presence of heparin, inhibitory effects of ulinastatin on trypsin were enhanced, whereas its effects on chymotrypsin and elastase were attenuated. These results suggest that the two functional domains in ulinastatin are differently affected by heparin.View full abstractDownload PDF (238K) -
Kazuo Sato, Fukuichiro Okumura, Yoshio Goshima, Takeaki Miyamae, Yoshi ...1993 Volume 62 Issue 1 Pages 119-122
Published: 1993
Released on J-STAGE: April 12, 2006
JOURNAL FREE ACCESSL-Dopa is a potentiator for presynaptic β-adrenoceptors. We studied whether L-dopa potentiates the activities of other presynaptic receptors to modulate the evoked noradrenaline (NA) release in rat hypothalamic slices. UK14304 (0.1-1 μM), a selective α2-agonist, concentration-dependently inhibited NA release. Noneffective 10 pM L-dopa potentiated the UK14304-induced inhibition. This potentiation was selectively antagonized by 1 nM L-dopa methyl ester, a competitive L-dopa antagonist, while yohimbine antagonized both the inhibition by UK14304 alone and its potentiation by L-dopa. However, 10 pM L-dopa produced no effect on angiotensin II (0.1-1 nM)-induced facilitation. L-Dopa potentiates activities of presynaptic β- and α2-adrenoceptors but not those of angiotensin II receptors on rat hypothalamic NA neurons.View full abstractDownload PDF (267K)
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