Renal vascular reactivity in the bile duct-ligated rat

The renal dysfunction associated with liver disease appears to be caused by decreased renal perfusion. Altered renal vascular reactivity (RVR) may contribute to the development of decreased renal blood flow. This study was undertaken to assess the effect of bile duct ligation (BDL) on RVR to norepinephrine and angiotensin II in the rat and to evaluate the role of prostaglandins in the modulation of altered RVR. Male Sprague-Dawley rats underwent either sham operation (SO) or BDL. Four days later, isolated kidney perfusions were established. Dose-response curves to norepinephrine (SO, n = 9; BDL, n = 10) and angiotensin II (SO, n = 7; BDL, n = 9) were obtained. The perfusate was modified to contain indomethacin, 10(-6) mol/L, and dose-response curves to norepinephrine (SO, n = 10; BDL, n = 8) and angiotensin II (SO, n = 4; BDL, n = 8) were obtained as well. Baseline resistances did not differ between any of the groups. RVR to norepinephrine did not appear to be altered by BDL; however, increased RVR to norepinephrine was unmasked by inhibition of prostaglandin synthesis. BDL did not affect the RVR to angiotensin II with or without indomethacin. BDL is associated with an increase in renal vascular sensitivity to norepinephrine, which is balanced by a compensatory increase in renal prostaglandin activity in response to norepinephrine stimulation. These findings are consistent with theories that decreased renal perfusion associated with liver disease may be mediated by catecholamines.