Mechanism of altered glomerular hemodynamics during chronic sodium depletion

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Abstract
Chronic sodium depletion in the rat is associated with decreased nephron filtration rate (SNGFR), nephron plasma flow (rpf), and a reduction in the glomerular permeability coefficient (LpA). This study was designed to determine whether the reduction in LpA could be acutely reversed with volume repletion and whether administration of angiotensin I converting enzyme inhibitor will restore LpA to normal values in the sodium-depleted rat. Measurements were performed in Munich-Wistar rats employing micropuncture techniques to assess the effects of acute volume repletion, 3-5 days of oral converting enzyme inhibitor (CEI) (30 mg . kg body wt-1 . day-1), and longer term (13-18 days) treatment with CEI begun just before or after initial volume depletion. Volume repletion in chronic sodium-depleted rats restored LpA to normal control values within a 60-min period, and values for glomerular dynamics were not different from a group of normal NaCl-intake rats to which the same treatment was applied. Both short-term and long-term CEI treatment during sodium depletion resulted in restoration of rpf to values not different from those with normal NaCl intake. However, only long-term but not short-term CEI treatment restored LpA to normal values. These studies suggest that intrarenal angiotensin II may mediate this reduction in LpA during chronic sodium depletion, but an effect of adrenergic nerve activity has not been excluded.