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Effects of mastoparan on a vascular contractility in rabbit aorta

Authors
 Young Ho Lee  ;  Sung In Kang  ;  Duck Sun Ahn  ;  Hye Young Lee  ;  Eun Jin Choi  ;  Bok Soon Kang 
Citation
 YONSEI MEDICAL JOURNAL, Vol.36(3) : 262-270, 1995-04 
Journal Title
YONSEI MEDICAL JOURNAL
ISSN
 0513-5796 
Issue Date
1995-04
MeSH
Animals ; Aorta / drug effects* ; Aorta / physiology ; Arginine / analogs & derivatives ; Arginine / pharmacology ; Calcium / metabolism ; In Vitro Techniques ; Indomethacin / pharmacology ; Intercellular Signaling Peptides and Proteins ; Neomycin / pharmacology ; Nitroarginine ; Peptides ; Quinacrine / pharmacology ; Rabbits ; Vasoconstriction / drug effects* ; Wasp Venoms / pharmacology*
Keywords
Mastoparan ; vascular contractility ; rabbit aorta
Abstract
Mastoparan is an amphiphilic tetradecapeptide derived from wasp venom which activates G-proteins. Several secondary effects have been attributed to this peptide, including activation of phospholipase and phosphatidylinositol kinase. The aim of the present study was to investigate the effects of mastoparan on vascular contractility. Rabbit aortic rings were cut and mounted on a force transducer to record isometric tension on a polygraph. The effects of mastoparan were then investigated on the contractile responses in the isolated rabbit aorta with or without endothelium. The results were summarized as follows; 1. Mastoparan caused biphasic response, a transient relaxation followed by a further contraction, in norepinephrine (NE)-precontracted ring with endothelium. These effects were not observed in the aorta in the absence of endothelium. 2. Mastoparan-induced transient relaxation was significantly inhibited by treatment with a N-ω-nitro-L-arginine or methylene blue. 3. When an inhibitor of phospholipase C, neomycin was added to the precontracted aortic ring with NE, the transient relaxation induced by mastoparan was inhibited, but sustained contraction was not inhibited. 4. When an inhibitor of phospholipase A2, quinacrine and inhibitor of the cyclooxygenase pathway, indomethacin, were added to a precontracted ring with NE, the transient relaxation induced by mastoparan was not inhibited, but sustained contraction was inhibited. 5. Mastoparan induced a contraction of the aorta either with or without endothelium. Indomethacin and nifedipine inhibited mastoparan-induced contraction. From the above results, we concluded that mastoparan acts on the endothelium and modifies the release of endothelium-derived relaxing factors such as nitric oxide and also endothelium-derived contracting factors such as metabolites of arachidonic acid.
Files in This Item:
T199500692.pdf Download
DOI
10.3349/ymj.1995.36.3.262
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/186656
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