Electrical properties of the rabbit cortical collecting duct from obstructed kidneys after unilateral ureteral obstruction. Effects of renal decapsulation.

Abstract

Ureteral obstruction causes impaired salt wastage and K+ secretion in the distal nephron segments, including the cortical collecting duct (CCD). Recently, we demonstrated that conductances of Na+ and K+ in the apical membrane, as well as the electrogenic Na+-K+ pump activity and the relative K+ conductance in the basolateral membrane of the collecting duct cell, were inhibited in the obstructed kidney after unilateral ureteral obstruction (UUO). To examine whether the increased intrarenal pressure might be causally related to these abnormalities in the CCD, the effects of unilateral renal decapsulation, a maneuver that partially blocks the increase in renal pressure, were evaluated with microelectrode techniques in isolated CCDs from UUO and sham-operated (control) rabbits 24 h after operation. Renal decapsulation had no effects on barrier voltages and conductances in the CCD from control animals. The lumen-negative transepithelial (VT) and basolateral membrane (VB) voltages as well as the transepithelial (GT) and the apical membrane (GA) conductances were decreased in the CCD from UUO animals compared with control animals. Pretreatment of renal decapsulation partially corrected the decreases in VT, VB, GT, and GA seen in the CCD from UUO animals. The changes in apical membrane voltage and GT upon addition of luminal amiloride and Ba2+, and the changes in VB upon addition of bath ouabain, were also decreased in the CCD from UUO animals compared with control animals. Pretreatment of renal decapsulation also partially corrected the above abnormalities seen in UUO animals, whereas it had no effect in control animals. The transference numbers for Cl-(tc) and K+ (tK) in the basolateral membrane were, respectively, increased and decreased in the CCD from UUO animals compared with control animals. Pretreatment of renal decapsulation also partially corrected the changes in tc, and tK seen in UUO animals, whereas it had no effect in control animals. We conclude that, in UUO animals, renal decapsulation partially corrects the inhibition of apical Na+ and K+ conductances as well as basolateral Na+-K+ pump activity and relative K+ conductance seen after UUO, whereas in control animals it has no

Rosiglitazone treatment attenuates renal tissue inflammation generated by urinary tract obstruction

“…The mechanism by which urinary tract obstruction culminates in partial or irreversible renal injury is incompletely understood. Following the onset of obstruction, there is an initial increase in pressure, proximal to the obstruction area, due to continued glomerular filtration 4,5 . However, renal injury may also progress independently of exaggerated intrarenal pressure.…”

“…Following the onset of obstruction, there is an initial increase in pressure, proximal to the obstruction area, due to continued glomerular filtration. 4,5 However, renal injury may also progress independently of exaggerated intrarenal pressure. The obstructed kidney has been demonstrated to release substances that are chemotactic for peripheral blood mononuclear cells, bringing about infiltration of the inflammatory cells into the site of injury.…”

α-MSH prevents impairment in renal function and dysregulation of AQPs and Na-K-ATPase in rats with bilateral ureteral obstruction

“…␣-MSH treatment also partly prevented the downregulation of AQP1 and Na-K-ATPase expression in rats after BUO-R for 48 h. In conclusion, ␣-MSH treatment significantly prevents impairment in renal function and also prevents downregulation of AQP2, AQP3, and Na-K-ATPase during BUO or AQP1 and Na-K-ATPase after BUO-R, demonstrating a marked renoprotective effect of ␣-MSH treatment in conditions with urinary tract obstruction. urinary tract obstruction; water channels; sodium pump; urinary concentrating defect URINARY TRACT OBSTRUCTION is associated with long-term impairment in the ability of the kidney to regulate urinary excretion of water and sodium (2,10,11,17,25,32). Hemodynamic changes are prominent, such as a reduction of renal blood flow (RBF) and glomerular filtration rate (GFR) (7, 31, 44).…”

Altered expression of epithelial sodium channel in rats with bilateral or unilateral ureteral obstruction

“…A marked and sometimes prolonged diuresis that is characterized by massive losses of sodium and water occurs after release of BUO (1,8,9,17,21,29). Previous studies using in vivo micropuncture techniques and in vitro isolated, perfused tubules from kidneys subjected to urinary tract obstruction demonstrated a striking impairment of fluid reabsorption in the proximal tubules, distal tubules, and the collecting duct (15).…”

“…Obstruction profoundly reduces the ability to concentrate and dilute the urine and reduces the ability of renal tubules to transport Na ϩ , K ϩ , and H ϩ (1,8,9,17,21,29). Release of obstruction results in a dramatic increase in renal sodium and water excretion (16,28,40).…”