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Volume 102, Issue 1
Displaying 1-5 of 5 articles from this issue
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Shigekatsu KOHNO, Katsuya OHATA1993 Volume 102 Issue 1 Pages 1-10
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe regulation of airway caliber is important for supporting the physiological respiratory function and is con sidered to be mainly controlled by the central and peripheral nervous systems. In the present review, we discussed the resting tonus of the isolated airway smooth muscle of the guinea pig and compared it with that of the human; the former is similar to the latter because both are well-developed in the airway and well-responsive to a variety of mediators. The resting tonus of the isolated guinea pig trachea is largely decreased by indomethacin, a cyclooxygenase inhibitor, while that of the isolated human bronchus is increased following transient decrease by indomethacin. Furthermore, the human bronchus is markedly decreased by not only a selective peptide leukotriene antagonist, MCI-826, but also 5-lipoxygenase inhibitors, AA 861 and cirsiliol. These results indicate that contractile prostanoid(s) and peptide leukotrienes are possible mediators for the maintaining the resting tonus of the respective preparations. Both preparations still have a small but substantial part of the resting tonus resistant to these drugs, the mediator(s) responsible for which is not clarified yet. In short, arachidonate metabolites are major candidates for the resting tonus of either isolated guinea pig or human airway smooth muscle and may contribute to at least a part of the regulation of the airway caliber as autacoids in vivo.View full abstractDownload PDF (19347K) -
Yoshio GOSHIMA1993 Volume 102 Issue 1 Pages 11-21
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSLevodopa was released by depolarizing stimuli from rat striata in a transmitter-like manner in vitro and in vivo. Exogenous nanomolar levodopa stereoselectively facilitated the release of dopamine and noradrenaline via presynaptic β-adrenoceptors in brain slices even under inhibition of aromatic L-amino acid decarboxylase. This facilitation was competitively antagonized by levodopa methyl ester, whereas it was non-competitively antagonized by propranolol. Furthermore, picomolar levodopa stereoselectively potentiated the isoproterenol-induced facilitation of the noradrenaline release. Levodopa methyl ester selectively antagonized this potentiation, while propranolol antagonized both the facilitation by isoproterenol alone and its potentiation by levodopa. The recognition site for levodopa could be differentiated from the carrier proteins for levodopa transport, because nanomolar levodopa methyl ester abolished the levodopa-induced facilitation of the noradrenaline release, whereas a 30 times higher concentration of L-phenylalanine or L-leucine produced no antagonism. Microinjection of levodopa into the nucleus tractus solitarii led to dose-dependent decreases in arterial blood pressure and heart rate in rats in a levodopa methyl ester-sensitive manner. Based on these findings, we propose that levodopa itself is an endogenous neurotransmitter in the CNS.View full abstractDownload PDF (24843K) -
Yoshiaki OKAMIYA, Tadashi KISHIMOTO, Kumiko AOKI, Kiyotaka SUNAKAWA, K ...1993 Volume 102 Issue 1 Pages 23-33
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe effects of palonidipine hydrochloride [TC-81: (±)-3-benzylmethylamino)-2, 2-dimethylpropyl methyl 4-(2-fluoro-5-nitrophenyl)-1, 4-dihydro-2, 6-dimethyl-3, 5-pyridinedicarboxylate hydrochloride], a new calcium antagonist, on the coronary artery were studied in dogs. In the isolated canine coronary artery, TC-81 inhibited high K+ (60 mM)-induced contraction in a concentration-dependent manner. The relaxant activity of TC-81 was equal to that of nicardipine and more potent than those of nifedipine and diltiazem. TC-81 increased coronary blood flow in a dose-dependent manner after i.v.-administration in anesthetized open-chest dogs. The activity of TC-81 was equal to that of nifedipine or nicardipine, but the duration of its effect was longer than that of nifedipine or nicardipine. By oral administration in conscious dogs, TC-81 increased coronary blood flow at 0.1 mg/kg or more, and its activity was 10 times more potent than that of nifedipine. These results suggest that TC-81 increases coronary blood flow and is capable of improving the oxygen supply-demand relationship during angina pectoris.View full abstractDownload PDF (21137K) -
Osamu YAOKA, Kazumi AOKI, Tohru NAKAJIMA, Michihide SETOGUCHI1993 Volume 102 Issue 1 Pages 35-45
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe antihypertensive activity of quinapril was examined in normotensive and various hypertensive animal models. In 2-kidney, 1-clip renal hypertensive rats (2K-RHR), quinapril (0.1 to 1.0 mg/kg, p.o.) had a dose-related and sustained antihypertensive action, which was as potent as that of enalapril and approximately 40 times stronger than that of captopril. Heart rate was not changed by these doses of quinapril. In spontaneously hypertensive rats (SHR) and 1-kidney, 1-clip renal hypertensive rats, quinapril as well as enalapril dose-dependently produced a significant fall in blood pressure. The relative potency and duration of the effect of quinapril was the same as that of enalapril in these models. Quinapril at 30 mg/kg, p.o. lowered blood pressure and increased heart rate in normotensive rats. In contrast, quinapril and enalapril failed to reduce blood pressure in DOCA/salt hypertensive rats. In the repeated dose study, no development of tolerance was observed during the administration period in 2K RHR and SHR. The antihypertensive effects in 2K RHR was greater than those in SHR. Quinapril was more potent and long-lasting than enalapril in 2K RHR and SHR. From these results, quinapril is expected to be useful for the clinical treatment of hypertension.View full abstractDownload PDF (25069K) -
[in Japanese], [in Japanese], [in Japanese]1993 Volume 102 Issue 1 Pages 47-52
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSDownload PDF (16018K)
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