Adenosine does not mediate renal sodium retention and peripheral vasodilation elicited by partial portal vein ligation in rats
✍ Scribed by S Murakami; J F Bernardo; R A Branch; R Sabra
- Book ID
- 102243755
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 214 KB
- Volume
- 23
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
sodium retention, (2) a sodium-retaining factor acting This study was conducted to assess the role of adenodirectly on the renal tubule is responsible for sodium sine in the peripheral vasodilation and sodium retention retention. (HEPATOLOGY 1996;23:346-352.) that occurs after partial portal vein ligation (PVL) in the rat. The experiment was performed on day 1 after surgery when transient maximal sodium retention de-
The pathogenesis of renal sodium retention in associveloped and day 7 when rats returned to sodium balation with liver disease has not been completely and ance. Hemodynamic studies were conducted under anesclearly defined. It is difficult to discriminate the comthesia in portal hypertensive rats with sodium retention plex contribution of multiple factors because the comand in sham-operated controls. Measurements were obmonest chronic liver disease, cirrhosis, is associated tained before and after administration of a nonselective with changes in hepatic architecture, which leads to A 1 and A 2 adenosine receptor antagonist 1,3-dipropyl-8change in hemodynamics as well as change in function.
p-sulfophenylxanthine (DPSPX) (10 mg/kg intravenously followed by 150 mg/min). Under baseline condi-Partial portal vein ligation (PVL) has been used to intions, portal hypertensive rats with sodium retention vestigate the contribution of individual mechanisms as were hypotensive, with decreases in total peripheral rean example of a simplified model of prehepatic portal sistance and filtration fraction on day 1 in comparison hypertension in which a hyperdynamic circulation is with the control group. Although hyperdynamic circulaassociated with sodium retention. This sequence is tion was still maintained by day 7, there was a return thought to mimic several hemodynamic abnormalities to sodium balance. The adenosine receptor antagonist and sodium retention observed in cirrhosis. [1][2][3][4][5][6][7][8] Even in had a modest vasoconstrictor effect on systemic and rethis model, intensive investigation has not elucidated nal vasculature in both groups, but less in portal hyperthe mechanism involved in causing peripheral vasoditensive rats. However, no change in glomerular filtralation and sodium retention. 2,[7][8] The hyperdynamic cirtion rate was observed. DPSPX induced a natriuresis in control rats (from 0.40 { 0.11 to 5.97 { 0.61 mEq/min on culation in this model has been attributed to splanchnic day 1, from 0.48 { 0.20 to 6.34 { 0.45 mEq/min on day 7). vasodilation rather than hepatic dysfunction. 3,4 In ad-This response was attenuated in portal hypertensive dition to the decrease in peripheral vascular resistance, rats on day 1 (from 0.14 { 0.04 to 1.67 { 0.57 mEq/min) arteriovenous shunts and tissue hypoxia have been but not on day 7 (from 0.20 { 0.06 to 5.11 { 0.55 mEq/ shown to develop in several vascular beds in both cirmin). These results suggest that in portal hypertensive rhosis and this model. [9][10][11][12] Partial occlusion of hepatic rats (1) adenosine is not responsible for vasodilation and blood flow might be expected to cause not only hemodynamic changes but also hepatic parenchymal hypoxia and alteration of liver function, particularly in the Abbreviations: PVL, portal vein ligation; DPSPX, 1,3-dipropyl-8-p-sulfoearly phase of this model. 8 Thus, many of the factors phenylxanthine; CrCl, creatinine clearance; FENa, fractional sodium excrepresent in cirrhosis are also present in the PVL model, tion; MAP, mean arterial pressure; CO, cardiac output; CI, cardiac index; TPR, total peripheral resistance; GFR, glomerular filtration rate; FF, filtration and it is possible that tissue hypoxia and changes in fraction; RBF, renal blood flow; Na Ex, sodium excretion rate; UV, urine volhepatic function might contribute to hemodynamic ume.
changes and renal sodium handling.