Vanadate causes synthesis of endothelium-derived NO via pertussis toxin- sensitive G protein in pigs

Ryuichi Nakaike, Hiroaki Shimokawa, M. Koji Owada, Osamu Tokunaga, Hiroshi Yasutake, Takuya Kishimoto, Chiharu Imada, Tadayoshi Shiraishi, Kensuke Egashira, Akira Takeshita

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

The effects of sodium orthovanadate, an inhibitor of protein tyrosine phosphatases, on the endothelial nitric oxide (NO) pathway were studied in vitro. Vanadate caused endothelium-dependent relaxations in isolated porcine coronary arteries, which were abolished by N(w)-nitro-L-arginine methyl ester. The relaxations were also abolished by pertussis toxin, an inhibitor of certain G proteins. Tyrosine kinase inhibitors, genistein and α-cyano-3- ethoxy-4-hydroxy-5-phenyl-methylcinnamamide (ST-638), significantly attenuated the vanadate-induced relaxations. Vanadate also caused pertussis toxins-sensitive, endothelium dependent relaxations in isolated porcine renal and femoral arteries and jugular veins. Immunoblots, using an antibody to phosphotyrosines and to c-Src in native porcine aortic endothelial cells, respectively, showed that vanadate induced an elevation of phosphotyrosine proteins and a decrease in the amount of the active form of c-Src family kinases; both changes were markedly suppressed by cotreatment with ST-638. These results indicate that in porcine blood vessels, vanadate causes a synthesis of endothelium-derived NO for which endothelial tyrosine kinases and pertussis toxin-sensitive G protein are considered to be closely involved.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume271
Issue number1 40-1
Publication statusPublished - Jul 1 1996

Fingerprint

Vanadates
Pertussis Toxin
GTP-Binding Proteins
Nitric Oxide
Swine
Phosphotyrosine
Protein-Tyrosine Kinases
Endothelium
Protein Tyrosine Phosphatases
Femoral Vein
src-Family Kinases
Genistein
Femur Neck
Jugular Veins
Renal Artery
Femoral Artery
Blood Vessels
Coronary Vessels
Endothelial Cells
Sodium

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Nakaike, R., Shimokawa, H., Owada, M. K., Tokunaga, O., Yasutake, H., Kishimoto, T., ... Takeshita, A. (1996). Vanadate causes synthesis of endothelium-derived NO via pertussis toxin- sensitive G protein in pigs. American Journal of Physiology - Heart and Circulatory Physiology, 271(1 40-1).

Vanadate causes synthesis of endothelium-derived NO via pertussis toxin- sensitive G protein in pigs. / Nakaike, Ryuichi; Shimokawa, Hiroaki; Owada, M. Koji; Tokunaga, Osamu; Yasutake, Hiroshi; Kishimoto, Takuya; Imada, Chiharu; Shiraishi, Tadayoshi; Egashira, Kensuke; Takeshita, Akira.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 271, No. 1 40-1, 01.07.1996.

Research output: Contribution to journalArticle

Nakaike, R, Shimokawa, H, Owada, MK, Tokunaga, O, Yasutake, H, Kishimoto, T, Imada, C, Shiraishi, T, Egashira, K & Takeshita, A 1996, 'Vanadate causes synthesis of endothelium-derived NO via pertussis toxin- sensitive G protein in pigs', American Journal of Physiology - Heart and Circulatory Physiology, vol. 271, no. 1 40-1.
Nakaike, Ryuichi ; Shimokawa, Hiroaki ; Owada, M. Koji ; Tokunaga, Osamu ; Yasutake, Hiroshi ; Kishimoto, Takuya ; Imada, Chiharu ; Shiraishi, Tadayoshi ; Egashira, Kensuke ; Takeshita, Akira. / Vanadate causes synthesis of endothelium-derived NO via pertussis toxin- sensitive G protein in pigs. In: American Journal of Physiology - Heart and Circulatory Physiology. 1996 ; Vol. 271, No. 1 40-1.
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