Shape and volume of living aldosterone-sensitive cells imaged with the atomic force microscope.

Abstract

The steroid hormone aldosterone, which is synthesized in the suprarenal glands and secreted in response to a reduction in circulating blood volume, increases water and sodium reabsorption in the kidney (,). Although kidney is the major target organ, various other cell types, including different epithelia, smooth muscle, and endothelium, respond to the hormone (, , , ). The acute aldosterone-induced responses of target cells are an intracellular calcium change and an intracellular pH increase (,,) along with activation of plasma membrane Na+/H+ exchange and plasma membrane proton conductance (,). Therefore, it is not surprising that researchers have postulated that these acute transmembrane shifts of electrolytes are accompanied by cell swelling (,). Cell swelling or shrinkage plays a critical role in endothelial cell (EC) function. ECs tightly coat the luminal surface of blood vessels, playing an important role in the regulation of vascular tone, in vascular remodeling, in the pathogenesis of arteriosclerosis, and in arterial hypertension of humans (). It has been shown that swelling of EC may disturb cell-to-cell interactions, resulting in an increase of transendothelial permeability, a precursor mechanism in the development of arteriosclerosis (,). Moreover, environmental stress (e.g., mechanical forces or hyperosmolarity) induces changes in cell volume and stimulates tissue plasminogen activator synthesis (, , , ). Direct evidence for the importance of cell-volume regulation of endothelial cells is the existence of a volume-sensitive protein kinase ().