Journal of Smooth Muscle Research
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Volume 44 , Issue 1
Showing 1-4 articles out of 4 articles from the selected issue
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Original
  • Elaine Campana Sanches Bornia, Valéria do Amaral, Roberto Barbo ...
    Type: Original
    Volume 44 (2008) Issue 1 Pages 1-8
    Released: May 14, 2008
    JOURNALS FREE ACCESS
    In endothelium-intact rat aortic ring preparations pre-contracted with norepinephrine or KCl, NG-nitro L-arginine (L-NOARG, 0.1 mM) and 1H-[1,2,4] oxidiazolo [4,3-a] quinoxalin-1-one (ODQ, 10 μM) antagonized the reduction of the vascular tone induced by stevioside, but this antagonism did not occur when the experiment was performed with endothelium-denuded aortic rings. The data indicates that the vasodilatation produced by stevioside is dependent on nitric oxide synthase and guanylate cyclase activities when the endothelium is not damaged.
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  • Hiroyasu Sakai, Maki Yamamoto, Yoshihiko Chiba, Miwa Misawa
    Type: Original
    Volume 44 (2008) Issue 1 Pages 9-16
    Released: May 14, 2008
    JOURNALS FREE ACCESS
    Although the role of protein kinase C (PKC) has been suggested in agonist-induced bronchial smooth muscle contraction, the PKC isoform(s) involved in this phenomenon is not clear now. In the present study, the effects of three PKC inhibitors, GF1092603X, Gö6976 and rottlerin on acetylcholine (ACh)-induced bronchial smooth muscle contraction were examined to identify the PKC isoform(s) involved in the contraction. Bronchial smooth muscles were pretreated with each PKC inhibitor (10-6 and 10-5 M) 30 min before cumulative administration of ACh. In another series of experiments, the effects of PKC inhibitors on the maximal contraction induced by 10-3 M ACh were determined: the inhibitors were cumulatively administered (10-8- 10-5 M) after the ACh-induced contraction reached plateau. The ACh-induced bronchial smooth muscle contraction was significantly inhibited by GF109203X (inhibitor of PKCα, β, γ, δ and ε) but not by Gö6976 (PKCδ, β and γ inhibitor) and rottlerin (PKCδ and θ inhibitor). Moreover, mRNA and protein of PKCε were detected in rat bronchial smooth muscle. Taken together, PKCε might be involved in the ACh-induced bronchial smooth muscle contraction in rats.
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  • Budbazar Enkhjargal, Michio Hashimoto, Hiroki Kinoshita, Yasushi Sakai
    Type: Original
    Volume 44 (2008) Issue 1 Pages 17-28
    Released: May 14, 2008
    JOURNALS FREE ACCESS
    The incidence of cardiovascular disease is markedly lower in cycling, pre-menopausal women and post-menopausal women receiving estrogen than in men or untreated post-menopausal women. Clinical studies demonstrate a protective role of estrogen in hormone replacement therapy in terms of reducing cardiovascular risk. However, the benefits of hormone replacement therapy in cardiovascular disease remain unclear. We investigated the effects of estrogen on the contractile responses of the renal artery of ovariectomized Wistar rats (OVX) compared to both ovariectomized 17β-estradiol-treated rats (OVXE) and sham-operated (control) rats. Isometric contraction of renal artery was recorded with a strain gauge transducer. The maximum contractile response of the renal artery smooth muscle to KCl (80 mM) in the OVXE group was significantly higher than that in both the control and OVX groups. The phenylephrine (PE) concentration-response curves in all three groups indicated a greater sensitivity at lower concentrations of PE following treatment with 100 μM L-arginine methyl ester (L-NAME). The EC50 values for PE in the three groups were 2 times lower in the presence of L-NAME than those lacking exposure to L-NAME. The EC50 value for PE in the OVX group was ~3 times lower in the presence of L-NAME than in those lacking exposure to L-NAME and 100 nM BMY 7378, an α1D-adrenoceptor antagonist. The rate of relaxation of the PE-induced contraction (T1/2) was significantly reduced in the OVX group relative to both the control and OVXE groups. T1/2 values after treatment with 100 μM L-NAME were slower than those lacking exposure to L-NAME in all groups. Further, the T1/2 value of the OVX group was 2 times greater than that of the control; this change was reversed in the OVXE group. In conclusion, our results suggest that estrogen regulates contraction and relaxation in the renal artery via NO synthase activity and alteration of the Ca2+ transport systems.
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  • Masaaki Higashihara, Mariko Watanabe, Shigeki Usuda, Kouji Miyazaki
    Type: Original
    Volume 44 (2008) Issue 1 Pages 29-40
    Released: May 14, 2008
    JOURNALS FREE ACCESS
    Myosin light chain genes of human hematopoietic cells have not been fully characterized. We previously reported the cloning of the full-length cDNAs of 20 kDa regulatory myosin light chain (MLC-2), named as MLC-2A, from Meg-01, a human megakaryoblastic leukemia cell line (J. Smooth Muscle Res. 37: 25-38, 2001). We now cloned another MLC-2 isoforms from human platelets and U937, a human monocytic leukemia cell line, named as MLC-2B and MLC-2C, respectively. Both MLC-2A and MLC-2B consisted of three exons, which were situated on gene loci 18p1.3. Analysis of the gene structure indicated that MLC-2A and MLC-2B utilized different exons. MLC-2C also consisted of three exons, which was situated on gene loci 20p12. Amino acid sequence of MLC-2C was, of interest, apparently almost the same as that of MLC-2 from chicken gizzard smooth muscle LC20-A (one amino acid's difference) and human vascular smooth muscle LC-20 (two amino acids' difference). All three protein kinase C phosphorylation residues (Ser-1, Ser-2, Thr-9) and both myosin light chain kinase phosporylation residues (Thr-18, Ser-19) are conserved in these three isoforms. The MLC-2A and MLC-2B mRNA were expressed constitutively in all of the human hematopoietic cell lines examined and their expression levels were almost the same. On the other hand, MLC-2C mRNA was expressed in untreated monocytic cell lines (U937 and A-THP-1) and HL-60 differentiated into monocyte/macrophage cell lineage by TPA treatment. These results indicate that smooth muscle type isoform, MLC-2C is the inducible isoform, and might play a crucial role in monocyte/macrophage cell lineage.
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