• Paolo Manunta, Elisabetta Messaggio, Nunzia Casamassima, Guido Gatti, Simona Delli Carpini, Laura Zagato, and John M Hamlyn.
• Scientific Institute San Raffaele, Università Vita-Salute San Raffaele, Via Olgettina 60, 20132 Milan, Italy. manunta.paolo@hsr.it
• Biochim. Biophys. Acta. 2010 Dec 1; 1802 (12): 1214-8.

AbstractThe Na(+) pump and its Endogenous modulator Ouabain (EO) can be considered as an ancestral enzymatic system, conserved among species ranging from Drosophila to humans, related to Na handling. In this review, we examine how EO is linked with vascular function in hypertension and if it impacts the pathogenesis of heart and renal failure. Moreover, the molecular mechanism of endogenous ouabain-linked hypertension involves the sodium pump/sodium-calcium exchanger duet. Biosynthesis of EO occurs in adrenal glands and is under the control of angiotensin II, ACTH and epinephrine. Elevated concentrations of EO and in the sub-nanomolar concentration range were found to stimulate proliferation and differentiation of cardiac and smooth muscle cells. They may have a primary role in the development of cardiac dysfunction and failure. Experimental data suggest that the Na/K-ATPase α(2)-catalytic subunit causes EO-induced vasoconstriction. Finally, maneuvers that promote Na depletion, as diuretic therapy or reduced Na intake, raise the EO levels. Taken together, these findings suggest a key role for EO in body Na homeostasis.Copyright © 2010 Elsevier B.V. All rights reserved.

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