Blunted pressure natriuretic response in the old rat: participation of the renal nerves

With advancing age, there is a generalized reduction in the ability of the kidney to generate a natriuretic response and, in addition, the incidence of salt-sensitive hypertension increases. One event that could link these changes is a defect that develops in the pressure natriuresis response of the old kidney. To test this possibility, we conducted studies on the anesthetized, male Sprague-Dawley rat to determine the effect of abrupt alterations of renal perfusion pressure (RPP) on urinary sodium excretion (U(Na)V). Young (3- to 5-month-old), middle-aged (11- to 13-month-old), and old (18 to 20-month-old) rats were studied, and RPP was varied by clamping the aorta during the infusion of a cocktail of vasoactive hormones that suppressed the activity of endogenous factors. The gain of the pressure natriuresis relationship was severely attenuated in the old rat compared with the young and middle-aged rats. This blunting of the pressure natriuresis relationship in the old rat was partially attenuated by acute renal denervation. This effect was not associated with marked alterations in the filtered load of sodium, implying that aging is associated with a loss of the tubular epithelial response to an acute change in RPP. These observations suggest that the blunted pressure natriuresis may have a role in the increased incidence of salt-sensitive hypertension and that increased renal nerve activity may have a contributory role.