L-Arginine-induced current in portal venous smooth muscle cells

• Published in: Journal of Smooth Muscle Research 2007, Vol.43(3), pp.109-116
• Main Authors: Kimura, Shinichi, Ohashi, Atsuko, Tohse, Noritsugu, Kitamura, Kenji, Shimamura, Keiichi
• Format: Article
• Language: English
• Subjects: Animals; Arginine - pharmacology; current; Female; In Vitro Techniques; L-arginine; Male; Membrane Potentials - drug effects; Muscle, Smooth, Vascular - cytology; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - physiology; Myocytes, Smooth Muscle - drug effects; Myocytes, Smooth Muscle - physiology; Na+; portal vein; Portal Vein - cytology; Portal Vein - drug effects; Portal Vein - physiology; rat; Rats; Rats, Wistar; smooth muscle; Vasoconstriction - drug effects; Vasoconstriction - physiology
• ISSN: 0916-8737; 1884-8796
• DOI: 10.1540/jsmr.43.109

In our previous report, we showed that L-arginine induced depolarization of smooth muscle cells of the rat portal vein with an increased contraction. To clarify the ionic mechanism of the membrane depolarization, the effect of L-arginine on the holding current was studied in freshly isolated smooth muscle cells of the rat portal vein. The whole-cell patch-clamp technique was used, with the membrane potential held at -60 mV. In the presence of Na+ in the perfusate, L-arginine 10 mM induced an inward current in about 50% of the cells. In Na+-deficient perfusate, L-arginine 10 mM increased the amplitude of the inward current in a Na+ concentration-dependent manner. BCH, an inhibitor of the Na+-dependent amino acid transporter, ceased the L-arginine-induced current. These results indicate that L-arginine induces an inward current via Na +-dependent mechanisms in rat portal venous smooth muscle cells.