NA+ REABSORPTION IN THE ISOLATED PERFUSED KIDNEY OF NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS AT DIFFERENT AGES

An intrinsic defect of renal Na+ excretion is postulated to play a role in the development of primary hypertension. As this defect may be masked in vivo by compensatory natriuretic mechanisms, the isolated perfused kidney model was used to study renal Na+ reabsorption at various stages in the development of primary hypertension. Isolated kidneys of 3- and 12-months-old spontaneously hypertensive rats of the Munster strain (SHR) and of age- and weight-matched normotensive rats (WKY) (n = 7 in each group) were perfused at constant pressure of 100 mmHg by a modified albumin-free Krebs-Henseleit solution. The fractional Na+ reabsorption, which is independent of GFR under these conditions, declined, as expected, in WKY and SHR kidneys during 90 min. of perfusion, due to deterioration of organ function. At any time of perfusion Na+ reabsorption was significantly elevated in SHR kidneys and 12-months-old WKY kidneys compared to 3-months-old WKY kidneys. Perfusion flow rates were not different between SHR and WKY kidneys. These data support the concept of an intrinsic renal defect in primary hypertension, which could also be important for the age-dependent increase in blood pressure.