Document Detail


Effect of a peptide inhibitor of protein kinase C on G-protein-mediated increase in myofilament Ca(2+)-sensitivity in rabbit arterial skinned muscle.
MedLine Citation:
PMID:  8012712     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. To investigate the role of protein kinase C in the increase mediated by guanosine 5'-triphosphate (GTP)-binding proteins (G-proteins) in the sensitivity of the contractile proteins to Ca2+ in vascular smooth muscle, the effect of a novel peptide inhibitor of protein kinase C (PKC19-36) on Ca(2+)-induced contraction and myosin light chain (MLC) phosphorylation was studied in the presence and absence of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) in beta-escin-skinned smooth muscle strips of rabbit mesenteric artery. For comparison, the effects were also observed of PKC19-36 on the action of phorbol 12,13-dibutylate (PDBu, an activator of PKC) on the two Ca(2+)-induced responses. 2. In beta-escin-skinned strips treated with ionomycin, Ca2+ (0.1-3 microM) concentration-dependently produced contraction in parallel with an increase in MLC-phosphorylation. GTP gamma S (10 microM) and PDBu (0.1 microM) each shifted both the Ca(2+)-force and Ca(2+)-MLC-phosphorylation relationships to the left without a significant change in either maximum response. The relationship between force and MLC-phosphorylation was not modified by either GTP gamma S or PDBu, indicating that the sensitivity of MLC-phosphorylation to Ca2+ is enhanced by both GTP gamma S and PDBu. 3. PKC19-36 itself modified neither the contraction nor MLC-phosphorylation induced by Ca2+ but it did block the PDBu-induced enhancement of these two Ca(2+)-induced responses. By contrast, PKC19-36 did not modify the GTP gamma S-induced enhancement of the two Ca(2+)-induced responses. Guanosine 5'-O-(2-thiodiphosphate) (GDP Beta S) attenuated the GTP gamma S-induced enhancement of the Ca2+-induced contraction.4. These results suggest that GTP gamma S increases Ca2+-induced MLC-phosphorylation through the activation of a PKC-independent mechanism and thus causes an increase in the sensitivity of the contractile proteins to Ca2+ in Beta-escin-skinned smooth muscle of rabbit mesenteric artery.
Authors:
T Itoh; A Suzuki; Y Watanabe
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of pharmacology     Volume:  111     ISSN:  0007-1188     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  1994 Jan 
Date Detail:
Created Date:  1994-07-25     Completed Date:  1994-07-25     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  311-7     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Binding Sites
Calcium / pharmacology*
Escin / chemistry
GTP-Binding Proteins / metabolism*
Guanosine 5'-O-(3-Thiotriphosphate) / pharmacology
Male
Mesenteric Arteries / drug effects
Microfilaments / drug effects*,  metabolism
Muscle Contraction / drug effects
Muscle, Smooth, Vascular / drug effects*,  metabolism
Myosins / metabolism
Peptide Fragments / pharmacology*
Phorbol 12,13-Dibutyrate / pharmacology
Phosphorylation
Protein Kinase C / antagonists & inhibitors*,  pharmacology*
Rabbits
Chemical
Reg. No./Substance:
0/Peptide Fragments; 0/protein kinase C (19-36); 37558-16-0/Phorbol 12,13-Dibutyrate; 37589-80-3/Guanosine 5'-O-(3-Thiotriphosphate); 6805-41-0/Escin; 7440-70-2/Calcium; EC 2.7.11.13/Protein Kinase C; EC 3.6.1.-/GTP-Binding Proteins; EC 3.6.4.1/Myosins
Comments/Corrections

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