Journal of Smooth Muscle Research
Online ISSN : 1884-8796
Print ISSN : 0916-8737
ISSN-L : 0916-8737
Volume 31, Issue 4
Displaying 1-7 of 7 articles from this issue
  • Jack A. Rall
    1995 Volume 31 Issue 4 Pages 117-118
    Published: 1995
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
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  • Takashi MORITA, Kazunori KIHARA, Hideki NAGAMATSU, Hiroyuki OSHIMA, Ta ...
    1995 Volume 31 Issue 4 Pages 119-127
    Published: 1995
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    Clenbuterol (10-10-10-7 M), a selective β2-adrenoceptor agonist, reduced spontaneous contractile force of isolated rabbit bladder dome, bladder base and proximal urethra. Clenbuterol inhibited both acetylcholine (Ach)-and electrical field stimulation (EFS)-induced contractions of rabbit bladder dome, but was more potent in inhibiting EFS-than Achinduced contractions. Acetylcholine-but not EFS-induced contractions in the bladder dome were completely inhibited by pretreatment with 10-6 M atropine. The atropine resistant component of the EFS-induced contractions was completely inhibited by tetrodotoxin, 10-6 M. Clenbuterol and a non-selective β-adrenoceptor agonist, isoproterenol, potentiated the EFS-induced contractions of isolated striated muscle preparations from the external urethral sphincter and from the extensor digitorum longus in the rabbit. Clenbuterol was more potent than isoproterenol in increasing EFS-induced contractile force in the external urethral sphincter, whereas isoproterenol was more potent than clenbuterol in increasing EFS-induced contractile force in the extensor digitorum longus. These data suggest that clenbuterol may have a role in the treatment of urinary incontinence by inhibiting the detrusor contraction and fascilitating the external urethral sphincter selectively.
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  • Masaomi TAJIMI, Masatoshi HORI, Minori MITSUI, Hiroshi OZAKI, Hideaki ...
    1995 Volume 31 Issue 4 Pages 129-142
    Published: 1995
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    In bovine tracheal smooth muscle, carbachol (CCh, 1μM) and high K+ (72.7mM) induced sustained increases in cytosolic Ca2+level ([Ca2+] i), myosin light chain (MLC) phosphorylation and force of contraction. Forskolin (FK, 1-10μM) inhibited the CCh-induced increase in [Ca2+MLC phosphorylation and force in parallel. In contrast, FK inhibited the high K+-induced contraction and MLC phosphorylation without changing [Ca2+]In the absence of extracellular Ca2+ (with 0.5mM EGTA), CCh (10μM) and caffeine (20mM) induced transient increase in [Ca2+] i and contractile force by releasing Ca2+from cellular store. FK strongly inhibited the CCh-induced Ca2+transient, but failed to inhibit the caffeine-induced Ca2+transient. In the absence of external Ca2+, 12-deoxyphorbol 13-isobutylate (DPB, 1μM) induced sustained contraction without increase in [Ca2+] and MLC phosphorylation. FK inhibited this contraction without changing [Ca2+] In permeabilized muscle, Ca2+induced contraction in a concentration-dependent manner. FK (10μM) and cAMP (1-100μM) shifted the Ca2+-force curve to the higher Ca2+levels. CCh with GTP, GTPyS or DPB enhanced contraction in the presence of constant level of Ca2+. Forskolin and cAMP also inhibited the enhanced contractions in the permeabilized muscle. In the permeabilized, thiophosphorylated muscle, ATP induced contraction in the absence of Ca2+. cAMP (300μM) had no effect on this contraction. These results suggest that forskolin inhibits agonist-induced contraction in tracheal smooth muscle by multiple mechanisms of action; 1) inhibition of MLC phosphorylation by reducing Ca2+influx and Ca2+release, 2) inhibition of MLC phosphorylation by changing the MLC kinase/phosphatase balance, and 3) inhibition of regulatory mechanism which is not dependent on MLC phosphorylation.
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  • Tadayoshi TAKEUCHI, Yuko FUKUNAGA, Fumiaki HATA, Osamu YAGASAKI
    1995 Volume 31 Issue 4 Pages 143-151
    Published: 1995
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    In order to clarify the involvement of cyclic AMP-dependent protein kinase (protein kinase A) in acetylcholine (ACh) release from myenteric plexus of guinea pig ileum, the effect of H-89, a specific inhibitor of protein kinase A, on the ACh release was investigated. H-89 (0.1-10μM) inhibited the spontaneous and nicotine-induced release of ACh in a concentration dependent manner. It at 1μM decreased both kinds of release of ACh to almost half of the control, but it did not affect the ACh release evoked by electrical field stimulation and by 5-hydroxytryptamine. H-89 had no significant effect on the indomethacin (IND), an inhibitor of PG synthesis, -insensitive component of the spontaneous and nicotine-induced release of, ACh. OP-41483, an analog of PGI, and forskolin, an activator of adenylate cyclase, reversed the inhibitory effect of IND on the ACh release. H-89 at 1μMcompletely inhibited the reverse effects of OP-41483 and forskolin. These results suggest that activation of protein kinase A is essential for modulation of the nicotineinduced and spontaneous ACh release from myenteric plexus of guinea pig ileum and the activity of protein kinase A is regulated by endogenous PGs via intracellular cyclic AMP level.
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  • Tatsuo GONDA, Hideo AKIYOSHI, Keiichi ICHIHARA
    1995 Volume 31 Issue 4 Pages 153-162
    Published: 1995
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    Three-dimensional structures of the nerves of the guinea-pig gallbladder, after histochemical demonstration of the acetylcholinesterase activity and HC1 hydrolysis-collagenase digestion, were examined by scanning electron microscope. HCl-collagenase digestion facilitated easy identification of silver and gold-intensified acetylcholinesterase-positive nerve fibers at a high accelerating voltage (25kV), due to their strong reflection image. Ganglia were either triangular or ovoidal in shape. Dense para and peri-vascular nerve fibers occurred around the cystic artery. There were a few intramuscular nerve fibers with varicosity-like structures among smooth muscle bundles. Dense branched and tapering nerve fibers with varicosities in the lamina propria mucosae were closely attached to epithelial cells. The acetylcholinesterase-positive fibers in the lamina propria and peri and para-vascular nerves, and fewer positive fibers in the smooth muscle layer probably represent cholinergic nerves involved in the concentration of biliary compounds and lesser in the motor function of the smooth muscle.
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  • Shimizu K., Kaneda T., Chihara H., Kaburagi T., Nakajyo S., Urakawa N.
    1995 Volume 31 Issue 4 Pages 163-173
    Published: 1995
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    A contractile propertiy of phenylephrine (PE), α1 agonist, on rat anococcygeus muscle was compared with that on rat aorta by simultaneously measuring changes in intracellular Ca2+ ([Ca2+] 1) level and muscle tension.(1) PE (0.1-30, μ M) and high K+induced a sus tained increases in [Ca2+] 1 level and muscle tension of both the muscles.(2) An application of verapamil (10μM) and EGTA (4mM) decreased the PE or high K+-increased tension and [Ca2+] 1 level in both the muscle, respectively.(3) A cumulative application of PE or high K+to anococcygeus muscle and aorta exhibited a positive relationship between [Ca2+] 1 and developed tension. The developed tension by PE was greater than that by high K+at the same level of [Ca2+] 1 only in the aorta. A difference of regression slopes in the relationship between [Ca2+] 1 level and muscle tension under PE and high K+-treatments in aorta was significant, but that in anococcygeus muscle was not.(4) An application of PE to anococ cygeus muscle in Ca2+free medium elicited a small transient contractile tension and increase in [Ca2+] 1 level, but that to aorta showed a large and transient increase in both the parameters.(5) Phorbol ester, DPB (1μM), did not affect muscle tension or [Ca2+] 1 level in anococcygeus muscle, but DPB induced greater increases in aorta.(6) An application of PE (10μM) with GTP produced a left shift in the pCa-tension curve in the β-escin-permeabilized fiber of the anococcygeus muscle.
    In summary, it is suggested that the sustained contraction induced by PE in anococ cygeus muscle is involved with the increases in [Ca2+] 1 which is due to Ca2+influx mediated by a, receptor, but scarecely to Ca2+release from the intracellular storage, and that an increase in Ca2+sensitivity to PE is found only in the permeabilized anococcygeus muscle. The Ca2+-independent contractile mechanism in PE response as seen in aorta is probably to be absent in anococcygeus muscle. Moreover, it seems that the effect of the drug acting protein kinase C on anococcygeus muscle is extremely lesser than that on aorta.
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  • Satoru ADACHI, Masataka OKU
    1995 Volume 31 Issue 4 Pages 175-187
    Published: 1995
    Released on J-STAGE: July 21, 2010
    JOURNAL FREE ACCESS
    Clarification of the mechanism of oxytocin (OT)-induced contraction of the uterus seems to be essential for the elucidation of the mechanism of the initiation of labor. Although it has been suggested that estradiol (E) and progesterone (P) are involved in the expression of oxytocin receptors (OTRs), no consensus opinion has been formed on this topic. Thus we recently assessed the effects of E and P on OTR expression using cultures of human uterine cells and we examined the changes in the expressed OTRs following treatment of the cell with exogenous OT. The following results were obtained:
    1. The total cellular concentration of OTRs as measured in the myometrial crude membrane fraction (total OTR concentration) showed an increase dependent on the E concentration and on the length of the incubation period in the presence of E. This increase following treatment with E (10-7M) was suppressed by simultaneous treatment with P in a concentration-dependent manner being suppressed by 50% when the concentration of P was 2.7×10-6M (E/P ratio=0.037). When 1nM OT was added to the culture, the total OTR concentration did not change within the first 30 minutes of incubation, but decreased by about 70% twenty-four hours after addition of OT.
    2. The concentration of OTRs at the cell surface (surface OTR concentration), as measured in myometrial cells that adhered to the culture plate, did not change with time when the cells were cultured at 4°C in the presence of 1nM OT. However, when cultured at 37°C, the surface OTR concentration showed decreases dependent on the concentration of OT added and the time after the addition of OT. This change was observed within 60 minutes after the addition of OT to the culture. This decrease in surface OTR concentra tion was suppressed by concanavalin A (ConA), an inhibition of the internalization of cellsurface receptors.
    These results indicate that in humans also, the expression of myometrial OTRs is regulated by change in the E/P ratio. The present study also revealed that OTRs, once expressed, soon disappear from the cell surface in the presence of exogenous OT (due to internalization of OTRs, i.e., dislocation of OTRs from the cell surface to the inside of the cells), and that prolonged exposure to OT even leads to the disappearance of intracellular OTRs. The present study thus suggests that the expression of human myometrial OTRs is regulated by E and P, and that an agonist-induced desensitization mechanism at the receptor level, similar to that reported for β-adrenergic receptors, is also operating in this receptor.
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