title: Role of renal sympathetic nerve activity in renal failure associated with obstructive jaundice in the rat.
abstract: The propensity for renal failure associated with obstructive jaundice and liver disease may be related to enhanced vasoconstriction of the renal vascular bed with resultant decreases in renal blood flow. Renal sympathetic nervous activity may be a mediator of this effect. The increased renal production of prostaglandins which has been observed in previous models of bile duct ligation may serve to counterbalance the effects of such vasoconstricting influences. This study was undertaken to assess the effect of bile duct ligation on renal function and prostaglandin production in the rat. Furthermore, this study was designed to determine if renal sympathetic nerve activity contributes to the development of renal failure after bile duct ligation. Sprague-Dawley rats underwent either sham operation (n = 8), bilateral renal denervation (n = 10), bile duct ligation alone (n = 11), or bile duct ligation and bilateral renal denervation (n = 10). Renal function was assessed before and 4 days after operation. Bile duct ligation resulted in a 46% decrease in creatinine clearance (p less than 0.01), a 33% decrease in urinary sodium excretion (p less than 0.01), a twofold increase in urine flow (p less than 0.01), and twofold increases in urinary excretion of PGE2, 6-keto-PGF1 alpha, and thromboxane B2 (p less than 0.01). Renal denervation did not prevent the decreases in creatinine clearance and sodium excretion seen after bile duct ligation and had no effect on the changes in urine flow and prostaglandin excretion. These findings demonstrate that bile duct ligation in the rat results in impaired renal function, accompanied by increases in renal prostaglandin production. In addition, this study indicates that the perturbations in renal function and renal prostaglandin production induced by bile duct ligation are not mediated by renal sympathetic nerve activity.
authors.affiliation: Department of Surgery, State University of New York--Health Science Center, Brooklyn.
authors.forename: P A
authors.initials: PA
authors.lastname: O'Neill
authors.forename: R B
authors.initials: RB
authors.lastname: Wait
authors.forename: K U
authors.initials: KU
authors.lastname: Kahng
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000818:Animals; D001652:Bile Ducts / Q000601:surgery; D002779:Cholestasis / Q000503:physiopathology*; D003714:Denervation; D015232:Dinoprostone / Q000652:urine; D007668:Kidney / Q000294:innervation* / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000503:physiopathology* / Q000652:urine; D007677:Kidney Function Tests; D008026:Ligation; D008297:Male; D011453:Prostaglandins / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013929:Thromboxane B2 / Q000652:urine
chemical_list: D011453:Prostaglandins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D015232:Dinoprostone