CULTURING INDUCED EXPRESSION OF BASOLATERAL NA-H+-2CL(-) COTRANSPORTER BSC2 IN PROXIMAL TUBULE, AORTIC ENDOTHELIUM, AND VASCULAR SMOOTH-MUSCLE()

So far, two isoforms of the neutral Na+-K+-2Cl(-) cotransporter have b een 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-sensit ive Rb-86(+) uptake studies. A surprising finding was the absence of B SC2 in fully differentiated freshly-isolated proximal tubule, porcine aortic endothelial cells, and rat vascular smooth muscle cells. Severa l studies have reported modulation of the cotransport activity by vaso active substances and suggested a role for disturbed cotransport in, f or example, the pathogenesis of essential hypertension. All these obse rvations, however, were made in cultured cells which, in view of our f indings, makes the physiological relevance questionable.