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Biomedical subjects

I Takayanagi

Publications and source records attributed to I Takayanagi.

At least 217 records · Page 12Linked to original sources
PubMed1983

Inhibitory action of 2-(1-,2-benzisoxazol-3-yl)-3-[2-(2-piperidinoethoxy) phenyl]acrylonitrile (SX-284) on acetylcholine release from vagus nerve in guinea pig ileum.

Newly synthesized compound, 2-(1-,2-benzisoxazol-3-yl)-3-[2-(2-piperidinoethoxy)phenyl]acrylonitrile (SX-284) inhibited electrically evoked acetylcholine release from the stores in the myenteric plexus-longitudinal strips of guinea pig ileum which was labelled with [3H]-choline but not the evoked release of tracer from rat vas deferens after labelling with [3H]-norepinephrine. These results support our previous findings that SX-284 specifically inhibit acetylcholine release from the vagus nerve in the gastrointestinal canal.

Acetylcholine↗
PubMed1983

Pharmacological characterization of ionophore X537A-induced contractile responses in isolated rabbit taenia coli and aorta.

Pharmacological action of ionophore X537A was studied in taenia coli and aortic strips isolated from rabbit. These isolated smooth muscle preparations contracted by X537A (10(-5)-10(-4) M). A removal of Ca ions from the buffer solution considerably reduced the contraction of taenia coli but not that of aorta. D 600 (methoxyverapamil, 10(-6) M) was without any effect in the contraction of both tissues by X537A (10(-4) M). However, papaverine (10(-4) M) and Aspaminol (1, 1-diphenyl-3-piperidinobutanol hydrochloride, 10(-4) M) inhibited X537A (10(-4) M)-induced contraction markedly in taenia coli but slightly in aorta. Inhibitory effects of these drugs were reversed in taenia coli by increasing Ca ion concentration in buffer solution but not in aorta. X537A (10(-4) M)-induced contraction of aorta was not affected by a pretreatment of rabbit with reserpine and preincubation of the isolated preparations with guanethidine (10(-6) M) or prazosin (10(-7) M). These results suggest that ionophore X537A might produce the contraction through an increase of Ca influx in isolated rabbit taenia coli which are little or not affected by D 600, whereas the contraction of rabbit aorta induced by X537A is mainly due to facilitation of release of Ca sequestered intracellularly.

Animals↗
PubMed1983

The actions of sodium nitroprusside and diltiazem on calcium-, potassium- and histamine-induced contractile responses in isolated rabbit basilar artery, aorta, taenia coli and tracheal smooth muscle.

The effects of sodium nitroprusside (NaNP) and diltiazem on CaCl2-,KCl- and histamine-induced contractile responses were studied in isolated rabbit basilar artery, aorta, taenia coli and trachea. NaNP reduced CaCl2-induced maximal contractions in basilar artery and aorta, but little affected those in taenia coli and trachea. NaNP reduced histamine-induced maximal contraction markedly in aorta but slightly in basilar artery and taenia coli. The reduction in aorta was reversed by increasing CaCl2 contraction in bathing medium. NaNP inhibited histamine-induced contractions of basilar artery, aorta and taenia coli in Ca-free medium. Diltiazem reduced CaCl2-induced maximal contractions in basilar artery and aorta, whilst it caused a parallel shift of concentration-response curves for CaCl2 to the right in taenia coli and trachea. diltiazem reduced histamine-induced maximal contractions in basilar artery and taenia coli. These reductions were reversed by increasing CaCl2 concentration in bathing medium. Diltiazem strongly inhibited histamine-induced contraction of taenia coli in Ca-free medium. The effects of NaNP and diltiazem on KCl-induced contractions both in normal (Ca; 2.5 mM) and in high Ca (Ca; 12.5 mM) media were also studied. From the results obtained in this study, the actions of NaNP and diltiazem were considered to vary with the type of smooth muscle or the condition eliciting contraction. Their possible mechanisms were discussed in this paper.

Animals↗
PubMed1983

A possible mechanism of action of a beta-adrenergic partial agonist (carteolol) in guinea pig taenia caecum.

Carteolol, 5-(3-tert-butylamino-2-hydroxy)propoxy-3, 4-dihydrocarbostyril hydrochloride was found to be a beta-adrenergic partial agonist in the taenia caecum of guinea pig. Concentration response curves of carteolol and isoprenaline were parallelly shifted by propranolol (10(-7) M) suggesting that site of action of both the drugs was the same beta-adrenoceptor. The pD2-values of carteolol obtained from the concentration action curves in mechanical response and increase of tissue concentration of cyclic AMP were significantly different from its pA2-value against isoprenaline and its pKi-value (negative log of its apparent dissociation constant). A possible explanation of our observation would seem to be as follows. Carteolol and isopranaline interact with the same beta-adrenoceptor where there may be two different sites: a binding site for agonist and binding site for antagonist.

Animals↗
PubMed1983

The actions of D 600, aspaminol and papaverine on calcium-, potassium- and histamine-induced contractions of isolated rabbit basilar artery, aorta, taenia coli and tracheal smooth muscle.

The effects of D 600, Aspaminol (1,1-diphenyl-3-piperidinobutanol hydrochloride) and papaverine on CaCl2-, KCl- and histamine-induced contractile responses of isolated rabbit basilar artery, aorta, taenia coli and tracheal smooth muscle were compared with each other. D 600 reduced CaCl2-induced maximal responses in basilar artery and aorta, and parallelly shifted the concentration-response curves for CaCl2 to the right in taenia coli and trachea. D 600 also reduced histamine-induced maximal contractions in basilar artery and taenia coli. These reductions were not reversed by increasing CaCl2 concentration in bathing fluids. High concentration of D 600 parallelly shifted the concentration-response curve for histamine to the right in aorta. Like D 600, Aspaminol, a nonspecific smooth muscle relaxant, parallelly shifted the concentration-response curve for histamine in aorta. Papaverine parallelly shifted the concentration-response curve for CaCl2 in taenia coli and reduced the maximal responses in other tissues. Papaverine also reduced histamine-induced maximal responses in basilar artery, aorta and taenia coli. Influences of these smooth muscle relaxants on histamine-induced contraction in Ca-free buffer solution and on KCl-induced contraction in normal and high Ca (Ca: 12.5 mM) buffer solution were also studied. From the results obtained in this study, the effects of smooth muscle relaxants are considered to vary with the type of smooth muscle or the condition eliciting contraction, and the possible mechanisms of the contractions were discussed.

Animals↗
PubMed1983

Relationship between intrinsic activity of beta-adrenoceptor agonist and amount of spare receptors in guinea pig taenia caecum.

Beta-adrenoceptor mechanisms were studied in the isolated guinea-pig taenia caecum. Isoprenaline, desisopropylprocaterol and carteolol relaxed guinea-pig taenia caecum, and their intrinsic activities (mean +/- S.E.) were 1.0, 0.95 +/- 0.03 and 0.61 +/- 0.08, respectively. The pD2 values (mean +/- S.E.) were 8.59 +/- 0.06 for isoprenaline, 7.94 +/- 0.21 for desisopropylprocaterol and 6.35 +/- 0.14 for carteolol. The beta-adrenoceptors in guinea-pig taenia caecum were irreversibly inactivated by photoaffinity labeling with isoprenaline (6 X 10(-6) M). Photoinactivation of beta-adrenoceptors caused a considerable parallel shift in the dose-response curve of isoprenaline. The decline of the dose-response curves of desisopropylprocaterol and carteolol without a preceding shift was observed after photoinactivation. Isoprenaline, desisopropylprocaterol and carteolol increased cyclic AMP levels in guinea-pig taenia caecum, and the pD2 values were 7.43, 6.97 and 5.96, respectively. When differences between the pD2 values for test drugs obtained from the mechanical responses and from the increases of cyclic AMP levels were calculated, the differences for isoprenaline was larger than those for desisopropylprocaterol and carteolol. The dose-response curves for relaxation and cyclic AMP level by isoprenaline were both shifted to the right as a result of prior incubation with carteolol. These results suggest that there are spare receptors for isoprenaline, but few for desisopropylprocaterol and carteolol in the smooth muscle.

Adrenergic beta-Agonists↗
PubMed1983

Relationship between synaptosomal calcium uptake and antinociceptive action of morphine.

We studied the relationship between inhibition of 45Ca2+ uptake and the antinociceptive action induced by morphine and effects of papaverine and 1,1-diphenyl-3-piperidinobutanol hydrochloride (Aspaminol) on both these actions of morphine. Addition of these drugs in the incubation medium significantly inhibited glutamate-stimulated synaptosomal 45Ca2+ uptake. The inhibition curves of morphine and Aspaminol on glutamate-stimulated synaptosomal 45Ca2+ uptake were linear, but that of papaverine was not. The inhibition of morphine on synaptosomal 45Ca2+ uptake was reversed by addition of naloxone. The inhibition of synaptosomal 45Ca2+ uptake induced by morphine was increased by the simultaneous addition of Aspaminol, but the inhibition induced by both morphine and papaverine was not increased to more than that by papaverine alone. Since morphine-antinociception was potentiated by Aspaminol and blocked by papaverine, these results support that the inhibition of synaptosomal calcium uptake plays an important role in the production of morphine-antinociception. However, since the inhibition of synaptosomal 45Ca2+ uptake by morphine was less than that by both Aspaminol and papaverine, and papaverine blocked morphine-antinociception, notwithstanding that 10(-4) M of papaverine alone completely inhibited glutamate-stimulated 45Ca2+ uptake into synaptosomes, it may be difficult to account for the antinociceptive action of morphine by the inhibition of 45Ca2+ uptake only.

Analgesia↗
PubMed1983

[Effect of suloctidil on the contractions of isolated rat aortic strips induced by norepinephrine and CaCl2].

The mode for the antispasmodic action of suloctidil was examined using aorta strips of rats in vitro. Both 10 microM suloctidil and 0.1 microM verapamil non-competitively inhibited the norepinephrine (NE)-induced contraction, of which pD'2 values were 4.61 +/- 0.41 and 6.16 +/- 0.22, respectively. Prazosin at 1 nM competitively inhibited the NE-induced contraction, and its pA2 value was 9.84 +/- 0.15. In the depolarized aorta, suloctidil competitively inhibited the CaCl2-induced contraction at the concentrations of 0.1 and 1.0 microM, of which the pA2 value was 5.96 +/- 0.26. However, 10 microM suloctidil inhibited the CaCl2-induced contraction in a non-competitive manner, and its pD'2 value was 5.01 +/- 0.14. The pA2 values for papaverine, verapamil and cinnarizine were found to be 5.23 +/- 0.10, 7.53 +/- 0.09 and 7.11 +/- 0.11 in CaCl2 induced contraction, respectively. In a Ca2+ free medium, 1 microM NE caused a transient contraction, which was maximum (23.8 +/- 2.2% of that in a normal solution) at 0.4 min after the application of NE. Subsequent application of 2.5 and 10 mM CaCl2 evoked a gradual contractile response, of which the maximum was 103.1 +/- 4.2% and 133.8 +/- 10.3% of that in a normal solution, respectively. Initial phasic contraction induced by NE in a Ca2+ free medium was not affected by 10 microM suloctidil nor by 0.1 microM verapamil, while this contraction was significantly suppressed by 1 nM prazosin. The tonic contraction, however, induced by re-application of CaCl2 was significantly suppressed by 10 microM suloctidil, 0.1 microM verapamil and 1 nM prazosin. Furthermore, 1.0 microM suloctidil and 0.1 microM verapamil significantly suppressed the 45Ca uptake into the depolarized aorta 5 and 10 min after the addition of 45CaCl2. On the contrary, suloctidil had no influence on the phosphodiesterase activity prepared from the aorta of rats even at 10 microM, whereas 1.0 microM papaverine inhibited the enzyme activity. It is concluded that suloctidil and verapamil inhibit the contractions of the isolated rat aorta induced by NE and CaCl2 through the inhibition of the influx of Ca2+ without affecting the intracellular Ca2+ release.

Animals↗
PubMed1983

Mechanical responses and calcium movements in rabbit iris smooth muscles.

Ca movements in mechanical responses of the isolated sphincter and dilator muscles of the rabbit iris to some drugs were studied. D600, a Ca-blocker, was practically ineffective in doses which relax the vascular and intestinal smooth muscles, while other smooth muscle relaxants were effective on the iris muscles in the same doses as used for other smooth muscles. The contractile responses of both iris smooth muscles to K+ and acetylcholine were immediately abolished by Ca removal from the bath fluid, suggesting that these contractile responses were due to Ca influx. Furthermore, Ca-channels studied seem to be uninfluenced by D600. A residual response to norepinephrine was observed in the iris dilator muscle immersed in the Ca-free solution and the contractile response of the skinned fiber of this muscle to norepinephrine was also obtained at a low Ca solution. Accordingly, contraction of the dilator muscle by norepinephrine seems to be due mainly to a facilitation of the release of intracellularly sequestered Ca.

Acetylcholine↗
PubMed1982

Contractile response of rabbit dilator pupillae muscle to isotonic high K or norepinephrine, and Ca movement.

Isotonic 80 mM K and norepinephrine contracted the isolated dilator pupillae muscle of the rabbit. Norepinephrine-induced contraction was inhibited by papaverine, but not by Ca blockers, while K-induced contraction was abolished by removing Ca from the bathing fluid but there was a residual response to norepinephrine in Ca-free solution. These results suggest that, in the rabbit dilator pupillae muscle, K-induced contraction is mainly attributable to the increase of Ca influx, while norepinephrine-induced contraction is mainly due to the facilitation of release of intracellularly sequestered Ca.

Animals↗
PubMed1982

Photoaffinity labeling of opioid receptor with morphine-7,8-oxide (morphine epoxide).

The opioid receptor mediating inhibitory action of morphine in the electrically stimulated guinea pig ileum was irreversibly photoinactivated by morphine epoxide (3 X 10(-6) M). Morphine epoxide (up to 3 X 10(-5) M) did not influence the responses of rat vas deferens (epsilon-receptor) or rabbit vas deferens (kappa-receptor) to electrical stimulation. Effective concentrations of morphine epoxide were much lower in the guinea pig ileum (mu-receptor) than in the mouse vas deference (delta-receptor). The inhibitory action of [Met]-enkephalin on the twitch responses of the rat vas deferens and mouse vas deferens to electrical stimulation were not influenced after irradiation in the presence of morphine epoxide (3 X 10(-6) M). Therefore, morphine epoxide is probably a useful probe for photoaffinity labeling of the mu-receptor in vitro.

Affinity Labels↗
PubMed1982

Photoaffinity labelling of dopamine receptors in molluscan smooth muscle.

Relaxation of catch contraction of the anterior byssus retractor muscle of the sea mussel Mytilus edulis L. by dopamine is mediated through a dopamine receptor but not through adrenoceptors (Takayanagi et al 1981). Photoaffinity labelling is a technique widely used in biochemical in vitro studies to test an interaction between a ligand and its binding site. Therefore, we tried photoaffinity labelling of the dopamine receptor in order to study the dopamine receptor in the anterior byssus retractor muscle of M. edulis. Sea mussels, collected from the east coast of Tokyo Bay were stored in aerated seawater (NaCl 456, KCl 11, CaCl2 2H2O 11, MgCl2 6H2O 48 nM and Tris-HCl 25 mM; pH 7 . 8 to 8 . 0) at 10 degrees C and used within a week of collection. Muscle bundles (about 1 mm in diameter) were dissected from the anterior byssus retractor muscle and suspended in a 10 ml organ bath filled with artificial seawater bubbled with air and kept at 24 to 25 degrees C. Responses to drugs were recorded isotonically under a tension of 0 . 2 g. After the muscle had been exposed to acetylcholine (10(-4)M) for 2 min to induce catch contraction and washed with artificial seawater for 5 min, dopamine was applied. Relaxations following a 10 min exposure to various doses of dopamine were estimated. The response to 3 x 10(-7) M dopamine was considered as the maximum response to obtain dose-response curves (Takayanagi et al 1981). To irradiate the muscle, a Toshiba lamp FL-20E (wavelength: 270 to 350 nm) was used as a light source. The muscle, immersed in artificial seawater containing dopamine (10(-4)M), was irradiated (1 cm from the lamp) for 25 min and then washed with artificial seawater for 60 min (Takayanagi et al 1976). After the muscle was irradiated in the presence of dopamine (10(-4)M) for 25 min and washed for 60 min, the dose-response curve of dopamine was shifted in a parallel way towards doses about 8 times higher (Fig. 1). This inhibition of dopamine-induced responses continued for at least 2 h. The dose-response curve for dopamine was unaffected when the muscle was incubated with both dopamine (10(-4)M) and haloperidol (10(-4)M) for 25 min under the irradiation conditions (Fig. 1). However, the inhibitory action of dopamine was unaffected when the muscle was irradiated in the absence of dopamine and washed for 60 min, suggesting that 20 min irradiation did not influence mechanisms for relaxation of this smooth muscle by dopamine. Furthermore, when the muscle was incubated with dopamine (10(-4)M) or haloperidol (10(-4)M) for 25 min and washed with artificial sea water, the dose-response curve for dopamine was not influenced. When promethazine (10(-4)M), an antihistamine drug found to have no antidopaminergic action in this muscle (Yoshida et al 1981), was used instead of haloperidol (10(-4)M), the dose response curve for dopamine was shifted after irradiation (data not shown). These results indicate the possibility that dopamine is photolysed to a reactive compound which reacts irreversibly with the dopamine receptor.

Affinity Labels↗
PubMed1982

Relationship between the Ba-induced contraction and cyclic AMP levels in the isolated longitudinal smooth muscle from guinea pig ileum.

Relationship between contraction and cyclic AMP levels induced by BaCl2 was examined in the longitudinal smooth muscle isolated from guinea pig ileum. BaCl2 3 X 10(-3)M caused a fast initial contraction, often followed by a gradual decrease of the contractile state. There was an increase in the tissue cyclic AMP 7 min or 14 min after the application of Ba. A phosphodiesterase activator imidazole reinforced the later phase of contraction by Ba and inhibited the increase in cyclic AMP. These results indicate that there is still a positive correlation between relaxation and increase in cyclic AMP and that an inhibitory action mediated by cyclic AMP is veiled behind the Ba contraction. Furthermore, these results may be interpreted by assuming that strong Ba contraction operates a feedback mechanism and that the feedback mechanism is associated with cyclic AMP increase. Indomethacin, an inhibitor of prostaglandins synthesis, little influenced the Ba-induced increase in cyclic AMP and rather inhibited the Ba contraction. Propranolol, a beta-adrenergic blocking agent, failed to exert influence on the Ba contraction. Based on these facts, it is suggested that the increase in cyclic AMP is not mediated by prostaglandins or catecholamines.

Animals↗
PubMed1982

Some pharmacological properties of morphine-7,8-oxide (morphine epoxide).

Morphine-7,8-oxide (morphine epoxide) is assumed to be a metabolite of morphine. Morphine epoxide in antinociceptive action was practically as potent as morphine. The development of tolerance in antinociceptive action was slower in the rats treated with morphine epoxide than in the rats with morphine. Furthermore, morphine epoxide was less potent than morphine in the inhibition of abstinence syndrome.

Analgesics↗