ABSTRACT
K. SHIMAMURAl'2•*, S. KIMURA \ A. OHASHI1, M. TOBA \ S. OKUNO \ Y. KANAMARU3 and H. SAITO4 1 Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, 1757 Kanazawa, Ishikari-Tobetsu, Hokkaido 061-0293, Japan
2 The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido, 1757 Kanazawa, Ishikari-Tobetsu, Hokkaido 061-0293, Japan
3 Aeromedical Laboratory, JASDF, 1-2-10 Tachikawa, Tokyo 190-8585, Japan Department of Basic Sciences, Japanese Red Cross Hokkaido College of Nursing, Kitami, Hokkaido 090-0011, Japan
Abstract-Changes in Na+-K+ pump activity influence intracellular Na+ and K+ concentrations. Activation of the electrogenic Na+-K+ pump hyperpolarizes plasma membrane and inhibits voltagedependent Ca2+ current. Na+-K+ pump activity has been shown to be inhibited in the absence of extracellular K+ or by cardiac glycosides. Involvement of Na+-K+ pump in regulation of cellular functions has been identified by inhibition of responses under inhibition of the Na+-K+ pump. In some smooth muscle tissues, responses to /J-agonists were inhibited by K+-free medium or ouabain, indicating that responses to ^-adrenoceptor agonists are mediated by the Na+-K+ pump. However, in other smooth muscle tissues, responses to /3-agonists were not inhibited by Na+-K+ pump inhibition. The Na+-K+ pump plays an important role in the regulation of circulatory function, and the levels of endogenous Na+-K+ pump inhibitors have been shown to be elevated in some types of hypertension. Endogenous Na+-K+ pump inhibitors possibly affect some of jS-adrenoceptor-mediated responses. Regulation of Na+-K+ pump may be important in the regulation of smooth muscle activity in normal conditions, as well as under pathophysiological conditions, such as hypertension.
