Culturing induced expression of basolateral Na+-K+-2Cl- cotransporter BSC2 in proximal tubule, aortic endothelium, and vascular smooth muscle.

So far, two isoforms of the neutral Na+K+-2Cl- cotransporter have been cloned in mammals. One isoform, BSC1, mediates apical ion entry in the renal thick ascending limb of Henle and a second, BSC2, appears to be an ubiquitously expressed Na+K+-2Cl- cotransporter. In primary cultures of rabbit proximal tubule, porcine aortic endothelial cells, and rat vascular smooth muscle cells, expression of the second isoform BSC2 was demonstrated by Northern blot analysis and bumetanide-sensitive 86Rb+ uptake studies. A surprising finding was the absence of BSC2 in fully differentiated freshly-isolated proximal tubule, porcine aortic endothelial cells, and rat vascular smooth muscle cells. Several studies have reported modulation of Na+K+-2Cl- cotransport activity by vasoactive substances and suggested a role for disturbed cotransport in, for example, the pathogenesis of essential hypertension. All these observations, however, were made in cultured cells which, in view of our findings, makes the physiological relevance questionable.