Renal interstitial pressure and sodium excretion during hilar lymphatic ligation.

Because lymphatic vessels drain the cortical interstitium of the kidney, lymphatic drainage might modulate cortical interstitial pressure and tubular Na+ reabsorption. We investigated the effects of short-term hilar lymph duct ligation in the rat on renal interstitial hydraulic pressure (assessed from subcapsular pressure), tubular Na+ reabsorption, and renal hemodynamics in the basal state and during volume expansion with saline. Subcapsular pressure was higher in lymphatic-ligated than in sham-operated kidneys both in the basal state (5.9 +/- 0.3 vs. 2.1 +/- 0.3 mmHg) and during short-term volume expansion (8.4 +/- 0.7 vs. 3.5 +/- 0.3). Compared with contralateral control kidneys, lymphatic ligation increased the basal urine flow (V) (1.76 +/- 0.2 vs. 1.18 +/- 0.2 microliter X min-1 X 100 g-1) and urinary Na+ excretion (UNaV) (0.10 +/- 0.03 vs. 0.05 +/- 0.02 mumol X min-1 X 100 g-1), but urea excretion, osmolar clearance, glomerular filtration rate, renal plasma flow, and filtration fraction were unchanged. The increases in V and UNaV with lymphatic ligation were not seen in salt-depleted rats but both were augmented by short-term volume expansion with saline. Sympathetic activation and inhibition by carotid occlusion and ganglionic blockade, respectively, elicited the same changes in vascular resistance in lymphatic-ligated and control kidneys. In conclusion, 1) lymphatic drainage is required to maintain a low renal cortical interstitial hydraulic pressure; 2) lymphatic ligation decreases Na+ and fluid reabsorption; 3) the natriuretic and diuretic effects of lymphatic ligation are not due to major changes in renal innervation or renal hemodynamics or to changes in osmolar or urea excretion but depend on the degree of extracellular fluid volume expansion.