Journal
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
Volume 14, Issue 1, Pages 51-57Publisher
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
DOI: 10.4196/kjpp.2010.14.1.51
Keywords
Calcium sensitization; Permeabilization; Mesenteric artery; Sodium fluoride; Rho kinase
Categories
Funding
- Korea Science and Engineering Foundation [R01-2008-000-12198-0]
- Ministry of Education. Science and Technology, Republic of Korea
- Brain Korea 21 Project
- National Research Foundation of Korea [R01-2008-000-12198-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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It was hypothesized that NaF induces calcium sensitization in Ca2+-controlled solution in permeabilized rat mesenteric arteries. Rat mesenteric arteries were permeabilized with beta - escin and subjected to tension measurement. NaF potentiated the concentration-response curves to Ca2+ (decreased EC50 and increased E-max). Cumulative addition of NaF (4.0, 8.0 and 1.6 mM) also increased vascular tension in Ca2+-controlled solution at pCa 7.0 or pCa 6.5, but not at pCa 8.0. NaF-induced vasocontraction and GTP gamma S-induced vasocontraction were not additive. NaF-induced vasocontraction at pCa 7.0 was inhibited by pretreatment with Rho kinase inhibitors H1152 or Y27632 but not with a MLCK inhibitor ML-7 or a PKC inhibitor Ro31-8220. NaF induces calcium sensitization in a Ca2+-dependent manner in beta-escin-permeabilized rat mesenteric arteries. These results suggest that NaF is an activator of the Rho kinase signaling pathway during vascular contraction.
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