Na+-K+ pump and Na+-K+ co-transport in cultured vascular smooth muscle cells from spontaneously hypertensive and normotensive rats
- 1 August 1992
- journal article
- molecular review
- Published by Wolters Kluwer Health in Journal Of Hypertension
- Vol. 10 (8)
- https://doi.org/10.1097/00004872-199208000-00006
Abstract
Objective This paper examines the hypothesis that aberrations in vascular smooth muscle univalent ion transport systems play an important role in the pathogenesis of hypertension. Design Baseline Na+-K+ pump and Na+-K+-2CI∼ co-transport activities and the regulation of these ion transport systems by angiotensin II and second messenger molecules have been studied in cultured aortic smooth muscle cells (VSMC) from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Methods Ion transport was studied using isotopic univalent cations (86Rb and 22Na). Results Baseline Na+- K+ pump activity was comparable between SHR- and WKY-derived VSMC. Baseline Na+-K+-2CI∼ and K+-CI∼∼ co-transport activity as well as K+ leakage were significantly greater in SHR VSMC. Baseline Na+-K+-2CI∼ co-transport was sensitive to inhibition by forskolin and ethyleneglycol-bis-(β-amino ethylester)-N,N,N′,N′-tetraacetic acid, whereas cyclic guanosine monophosphate and phorbol 12-myristate, 13-acetate had no effect. Angiotensin ll-stimulated Na+-K+-2CI∼∼ co-transport activity did not differ between WKY and SHR VSMC. Angiotensin II increased Na+- K+ -pump activity to a significantly greater extent in SHR VSMC. The stimulatory effect of angiotensin II upon Na+-K+ pump activity was reduced under Na+-free buffer conditions and in the presence of the Na+-H+ exchange inhibitor, ethylisopropyl amiloride. Na+-K+ pump activity was also stimulated by the protein kinase C activator, phorbol 12-myristate, 13-acetate, and this was completely inhibited under Na+-free buffer conditions. Conclusions SHR VSMC exhibit anomalous Na+-K+ -pump and Na+-K+-2Cl-co-transport activities. The influence of these univalent ion transport systems upon cellular Na+ and Ca2+ homeostasis invoke their participation in the pathogenesis of hypertension.Keywords
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