Role of Na+ and Ca2+ in stretch-induced Na+-K+-ATPase alpha -subunit regulation in aortic smooth muscle cells

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 274; no. 1; p. H83
• Main Authors: Liu, Xiang, Hymel, Lin J, Songu-Mize, Emel
• Format: Journal Article
• Language: English
• Published: United States 01.01.1998
• Subjects: Animals; Aorta - enzymology; Aorta - physiology; Calcium - metabolism; Calcium Channel Blockers - pharmacology; Calcium Channels - physiology; Calcium Channels, L-Type; Cells, Cultured; Gadolinium - pharmacology; Gene Expression Regulation, Enzymologic - drug effects; Gene Expression Regulation, Enzymologic - physiology; Isoenzymes - biosynthesis; Isradipine - pharmacology; Kinetics; Macromolecular Substances; Male; Muscle, Smooth, Vascular - enzymology; Muscle, Smooth, Vascular - physiology; Rats; Rats, Sprague-Dawley; Sodium - metabolism; Sodium-Potassium-Exchanging ATPase - biosynthesis; Stress, Mechanical
• ISSN: 0363-6135; 0002-9513; 1522-1539
• DOI: 10.1152/ajpheart.1998.274.1.H83

1  Department of Pharmacology and Experimental Therapeutics, Louisiana State University Medical Center, and 2  Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112 This study was designed to test the role of Na + and Ca 2+ entry in the stretch-induced Na + -K + -ATPase 1 - and 2 -isoform upregulation observed in our previous studies. We measured intracellular Na + in cyclically stretched rat aortic smooth muscle cells, with or without gadolinium treatment, for various durations and performed Western blotting to analyze the effects of stretch and the calcium channel blocker isradipine on the expression of -isoforms. Intracellular Na + was elevated significantly after 1- and 2-h stretch, but returned to baseline after 1-, 2-, and 4-day stretch. This increase in intracellular Na + was blocked by gadolinium. Both 1 - and 2 -isoforms were upregulated after either 2 or 4 days of cyclical stretch. Isradipine had no apparent effect on stretch-induced upregulation on either -isoform, thus suggesting that Ca 2+ entry through L-type channels is not involved in the stretch-induced upregulation. We therefore conclude that a transient intracellular Na + elevation during stretch may serve as a signal to mediate the 1 - and 2 -isoform upregulation. vascular smooth muscle cells; sodium-potassium-adenosinetriphosphatase -isoforms; isradipine; intracellular sodium; mechanical strain