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Volume 94 (1989)
- Issue 6 Pages 329-
- Issue 5 Pages 257-
- Issue 4 Pages 207-
- Issue 3 Pages 159-
- Issue 2 Pages 91-
- Issue 1 Pages 1-
Volume 94, Issue 6
Displaying 1-5 of 5 articles from this issue
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Makoto ENDO1989 Volume 94 Issue 6 Pages 329-338
Published: 1989
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSMechanisms and their pharmacology of Ca ion mobilization in skeletal, cardiac and smooth muscles are reviewed. In skeletal muscle, it is very likely that depolarization of T-tubule membrane causes conformational changes of dihydropyridine (DHP) receptors in the T-membrane, which in turn, most probably through some kind of protein-protein interaction, open the Ca2+ release channel in the sarcoplasmic reticulum (SR), the ryanodine receptor. Both the DHP receptor and ryanodine receptor have already been purified and sequenced, but the nature of the information transduction between these proteins still remains to be solved. Both of these proteins appear to have dual functions : the DHP receptor as a voltage sensor as described above and as a voltage-dependent Ca2+ channel and the ryanodine receptor as a physiological Ca2+ release channel and as a Ca2+-induced Ca2+ release (CICR) channel, an abnormality of which is known to cause malignant hyperthermia. In cardiac muscle, Ca2+ influx is essential not as the main Ca2+ source but to release Ca2+ from the SR, probably not through the CICR mechanism in the narrow sense but through a mechanism dependent on both Ca2+ and T-tubule depolarization. Several mechanisms of Ca2+ mobilization are used in smooth muscles and their features, different from those in striated muscles, are briefly reviewed.View full abstractDownload PDF (7958K) -
Hiroshi UEDA1989 Volume 94 Issue 6 Pages 339-349
Published: 1989
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSThe molecular basis of opioid receptor mechanisms was studied in reconstitution experiments using purified or membrane-bound opioid receptors and purified GTP-binding proteins (G-proteins). μ-Opioid receptor exclusively purified from rat brains was reconstituted with G-proteins in lipid vesicles. The μ-agonist stimulated the G-protein activity in both G, or Go-reconstituted vesicles. The stoichiometry revealed that one molecule of μ-receptor is functionally coupled to plural numbers of G, or Go molecules and that μ-preceptor exists in at least two different subtypes, μi and μo, separately coupled to Gi and Go, respectively. In addition, when the μ-receptor was phosphorylated by cAMP-dependent protein kinase, the μ-agonist-stimulation of G-protein activity disappeared, while the guanine nucleotide-sensitivity of agonist binding was unchanged. These findings suggest that there are independent domains in the receptor which are related to functional coupling to G-protein and to the agonist-binding modulation by G-protein. κ-Opioid receptor agonist inhibited the G-protein activity in guinea pig cerebellar membranes. Further experiments revealed that the κ-opioid receptor is functionally coupled to an inhibition of phospholipase C activity via an inhibition of Gi-activity. Such a receptor-mediated inhibition of G-protein activity may be the first demonstration of a signal transduction mechanism. The δ-opioid receptor agonist showed no effect on G-protein activity in guinea pig striatal and rat cortical membranes, while it stimulated it in NG108-15 cells. In all these membranes, the δ-agonist binding was markedly reduced by GTPγS in the presence of MgCl2. These findings suggest that δ-receptors in the brain might be coupled to G-protein without signal transduction.View full abstractDownload PDF (9182K) -
Shintaro NISHIO, Hirotoshi MATSUURA, Masakazu HATTORI, Takashi ENDOH, ...1989 Volume 94 Issue 6 Pages 351-361
Published: 1989
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSEffect of prostacyclin analogue, beraprost sodium (Sodium (±)-(lR*, 2R*, 3aS*, 8bS*)-2, 3, 3a, 8b-tetrahydro-2-hydroxy-l [(E)-(3S*)-3-hydroxy-4-methyl-l-octen-6-ynyl]-1H-cyclopenta[b]benzofuran-5-butyrate, TRK-100), on the cardiovascular system of the anesthetized dog was investigated. TRK-100 was injected intra-arterially and intravenously to study the vasodilating effect of the drug by a magnetic flow meter. Intra-arterial injection of TRK-100 augmented blood flow of vertebral, coronary, renal, supramesenteric, hepatic and femoral artery at a dose range of 0.0003 to 3, 000 μg/bed. The threshold doses of TRK-100 and PGI2 in the mesenteric artery were 0.003 μg and 0.0003 μg, respectively, and the same values were obtained in the splenic artery. Those were slightly lower than those of other arteries. Intravenous injection of TRK-100 augmented mesenteric and renal arterial flow to 193±30% and 118±4%, respectively. In this system augmentation of mesenteric and renal arterial flow was 179±19% and 135±1%, respectively, while vertebral, carotid, and femoral arterial flow decreased, respectively, to 71.4±2.1%, 80.0±9.4% and 61.4±5.6% by TRK-100 and 70.6±5.6%, 79.5±6.9% and 67.1±4.7% by PGI2. Inhibitory effects on heart functions such as cardiac output, left ventricular pressure, LV dP/dt, oxygen consumption, and cardiac work were seen. The effect was similar to PGI2. Coronary vascular resistance, total peripheral resistance and systemic blood pressure were also decreased by TRK-100 and PGI2.View full abstractDownload PDF (7545K) -
Yasushi MAGAMI, Takeshi AZUMA, Zenji SASAKI, Hideto INOKUCHI, Keiichi ...1989 Volume 94 Issue 6 Pages 363-369
Published: 1989
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSEffects of an anti-ulcer drug, 2'-carboxymethoxy-4, 4'-bis (3-methyl-2-butenyloxy) chalcone (sofalcone), on the generative cells and kinetics of superficial epithelial cells in mouse gastric mucosa, including the effect of hydrocortisone on them, were investigated by the use of 3H-thymidine auto radiography. The labeling indices and the width of the generative cell zone in the fundic mucosa were significantly decreased by administration of hydrocortisone. The decrease in the labeling indices and the width of the generative cell zone induced by administration of hydrocortisone were not inhibited by sofalcone. Hydrocortisone had no significant influence on the labeling indices of the generative cell zone in the pyloric mucosa, but decreased the width of it. The decrease in the width of the generative cell zone induced by hydrocortisone was inhibited by sofalcone. Concerning the influence on the kinetics of superficial epithelial cells, hydrocortisone inhibited the increase in the labeling indices of the superficial epithelial cells after continuous administration of 3H-thymidine in both the fundic mucosa and pyloric mucosa. In the fundic mucosa, sofalcone showed no influence on the inhibition by hydrocortisone, but in the pyloric mucosa, the effect of hydrocortisone was abolished by sofalcone. These results suggest that sofalcone inhibits the reduction of the cell production and the prolongation of the life span of superficial epithelial cells caused by hydrocortisone in the pyloric mucosa.View full abstractDownload PDF (7155K) -
Masao KOIDA, Hiromichi NAKAMUTA, Keiko MUGURUMA, Hiroshi SAKURAI, Yosh ...1989 Volume 94 Issue 6 Pages 371-377
Published: 1989
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSUsing isolated ring preparations of major arteries mainly of canine origin, we attempted to explore the mechanism of the vasodilating effect of naftidrofuryl oxalate (I) at the concentration of ?? 10μM. 1) The resting tension of canine carotid, femoral, coronary, renal and basilar arteries were not affected by I. 2) A weak or no papaverine-like activity was noted on coronary, renal and basilar arteries contracted by KCl (25 mM) or U46619 (20 nM). Porcine endothelin (30 nM)-induced contraction in the basilar artery also showed no response to I. 3) I produced a relatively strong anti-serotonergic effect in the basilar and femoral arteries, and the minimum effective concentrations of I for pretreating these arteries were 0.3 and 0.1 μM, respectively. I failed, however, to affect 8-OH-DPAT-induced contraction of the basilar artery. 4) In a low concentration such as 1 nM, I was able to release the vasodilating factor from the carotid artery. 5) The oscillatory contractions which developed in the rat thoracic aorta with phenylephrine (10μM) were not affected by I ( ?? 0.1μM). 6) Na oxalate ( ?? 1 mM) produced none of the effects of I described in 2) ?? 4). Based on the results obtained, it is concluded that I would exert its vasodilating effect not only directly via an anti-serotonergic action but also indirectly via its secretagogue-like action.View full abstractDownload PDF (5646K)
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