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Altered expression of renal apical plasma membrane Na⁺ transporters in the early phase of genetic hypertension

¹Chair of Nephrology, Second University of Napoli, Naples; ²Prassis Research Institute, Sigma-Tau, Milan; ³Laboratory of Environmental Physiology, Grange Blanche Faculty of Medicine, Lyon Cedex, France; ⁴Department of Physiology, University of Tuebingen, Tuebingen, Germany; and ⁵Chair of Nephrology, Ateneo Vita e Salute, S. Raffaele Hospital, Milan, Italy

Submitted 21 June 2004 ; accepted in final form 25 January 2005

The present study explores whether the development of hypertension in the Milan strain of rats (MHS) rats is preceded or paralleled by alterations of mRNA and/or protein levels of the major luminal Na⁺ transporters. MHS rats were studied at 23–25 days after birth; age-matched Milan normotensive (MNS) rats were used as controls. The glomerular filtration rate (GFR), measured by inulin clearance, was higher in MHS than in MNS rats, while the mean blood pressure was not different in the two strains of animals indicating that the MHS rats were still in the prehypertensive state. Type 3 sodium/hydrogen exchanger (NHE3), bumetanide-sensitive sodium-potassium-2 chloride cotransporter (NKCC2), sodium-chloride cotransporter (NCC) and -ENaC mRNA abundances were quantified by competitive PCR. In MHS compared with MNS, mRNA abundance was unchanged for NHE3 in proximal tubules, higher for NKCC2 in medullary thick ascending limbs of Henle's loops (TAL) and lower for NCC in distal convoluted tubules (DCT) and for -ENaC along collecting ducts (CD). Western blot experiments revealed 1) unchanged NHE3; 2) a significant increase in NKCC2 in the outer medulla; 3) a significant decrease in NCC in the renal cortex and of -ENaC in both the renal cortex and outer medulla, whereas - and -ENaC remained unchanged. These data indicate that, in MHS rats, there is a strong upregulation of NKCC2 along the TAL associated with increased GFR, robust inhibition of NCC cotransporter along the DCT and modest downregulation of -ENaC along the CD. The interplay of the various Na⁺ transporters may well explain why, at this age, the rats are still in the prehypertensive state.

type 3 sodium/hydrogen exchanger; sodium-potassium-2chloride cotransporter; sodium-chloride cotransporter; epithelial sodium channel; sodium; kidney

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