Intrarenal mechanisms of salt retention after bile duct ligation in rats.

Abstract

A B S T R A C T In order to study renal salt-retaining mechanisms during the early stages of ascites formation, rats were subjected to bile duct ligation. After this procedure, plasma volumes were found to be reduced and hematocrits slightly increased. The whole-kidney glomerular filtration rate and plasma flows were reduced to 59 and 57% of control values, but the filtration fraction was unchanged. Absolute sodium excretion, as well as the fraction of the filtered sodium load excreted, was also significantly reduced.When micropuncture techniques were used to examine the function of single superficial nephrons, the glomerular filtration rate in these nephrons was found to be reduced to 70% of controlled values, and fractional reabsorption was found to be increased at all accessible sites along the nephron. Filtration by intermediate and juxtamedullary nephrons, determined by Hanssen's technique, was reduced to 55 and 48% of control values.By the use of radioactive microspheres, it was demonstrated that blood flow to superficial, intermediate, and juxtamedullary nephrons was reduced to 49, 59, and 73% of control values. Filtration by superficial nephrons decreased much more than plasma flow-a finding which suggests that the measured increase in fractional reabsorption was associated with an increase in the superficial nephron filtration fraction.From this study, it appears that two factors play an important part in the sodium retention observed in the initial stages of ascites formation following bile duct ligation in rats: (a) a decrease in the filtered sodium Several parts of this manuscript have previously appeared in abstract form (Clin. Res. 22: 52A and 551A) and were presented to the Southern Sectional Meeting of the Ameri-

The use of microcomputed tomography to study microvasculature in small rodents

“…Selkurt and colleagues (87)(88)(89) showed that changes in renal perfusion pressure, within a range in which RBF remains unchanged (RBF autoregulation), were followed by dramatic changes in sodium excretion. This situation is comparable to that seen in the early stages of hepatic cirrhosis, where increased sodium reabsorption occurs without a change in RBF (2,12,79,104).…”

“…The increase in renal vascular resistance in patients with cirrhosis appears to mainly affect the superficial cortex, sparing medullary blood flow, as suggested by studies using either ultrasound (83,84) or xenon-washout techniques (52). Thus, because more of the RBF is shunted toward the deeper nephrons, which have an enhanced sodium reabsorbing capability, it is possible that this redistribution is contributing to the enhanced sodium and water retention that is typically seen in cirrhosis (104). In addition, changes in intrarenal blood flow may be implicated in the progression of human (79) and experimental cirrhosis (2, 12).…”

“…They suggested this shift to be the major explanation for the lack of urine flow, despite a preservation of renal blood flow (RBF). The shift of blood flow within the renal cortex from superficial short nephrons to deep long nephrons was later observed in sodium-retaining states such as cardiac insufficiency, hepatic cirrhosis, or hypovolemia (1,18,53,104). Selkurt and colleagues (87)(88)(89) showed that changes in renal perfusion pressure, within a range in which RBF remains unchanged (RBF autoregulation), were followed by dramatic changes in sodium excretion.…”

Renal Functional Alterations in Extrahepatic Cholestasis: Can Oxidative Stress Be Involved?

“…In the absence longed cholestasis, characterized by the reten tion of bile compounds, may cause renal dam age (reduction in renal hemodynamics, im pairment of renal excretion of water and salts and sensitization of the kidney to anoxic dam age) which sometimes leads to renal failure [1][2][3][4][5].…”

“…The pathophysiological cause of renal damage in the course of bile flow impairment is not well understood, even if several phe nomena, such as increased access of various bile constituents into the kidney (bilirubin and bile salts), have been suggested [1,3,5]. The nephrotoxic mechanism of these sub stances appears to be either indirect, because of their proinflammatory capacity (cytokines, acute-phase proteins, or leukocyte activation) or direct, because of hemolysis [6], Endotoxemia may also have a toxic effect on renal function; clinical and experimental works have focused on the role of endotoxins gut absorption in causing renal impairment during cholestasis, as well as in chronic renal failure [7][8][9][10].…”