Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to evaluate renal functional reserve (RFR) in obstructive nephropathy using amino acid loading and the effect of angiotensin converting enzyme (ACE) inhibitor on RFR. We divided 24 rabbits into 4 groups, consisting of a control, 6-hours-bilateral ureteral obstruction (BUO), 24-hour BUO and 24-hour BUO pretreated with ACE inhibitor. Following the ligation of the bilateral ureters at the vesicoureteral junction, a unilateral ureter was released after a 6-hour or 24-hour duration in the obstructive groups. We measured RFR and renal vascular resistance after releasing a unilateral ureter in BUO. The baseline GFR values in the 6-hour and 24-hour BUO groups were significantly lower than that in the control. RFR were 0.34 + 0.04 ml/min/kg (control), 0.10 + 0.03 (6-hour BUO), 0.01 + 0.03 (24-hour BUO) and 0.10 + 0.01 (ACE inhibitor), respectively. RFR in the 6-hour BUO group was well preserved compared with that in the 24-hour BUO group. Pretreatment with ACE inhibitor in the 24-hour BUO group enhanced RFR to the extent of 6-hour BUO. Our results demonstrated that angiotensin II plays an important role in decreased GFR with obstructive nephropathy. Moreover, the present data suggested that evaluation of RFR might play a key role in the recovery of the post-obstructive renal function.
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PMID:[Renal functional reserve in obstructive nephropathy]. 813 45

The renin-angiotensin system is well known to be involved in the pathophysiological changes in renal function after obstruction of the ureter. Previously, we demonstrated that bilateral ureteral obstruction (BUO) is associated with dramatic changes in the expression of both renal sodium transporters and aquaporin water channels (AQPs). We now examined the effects of the AT(1)-receptor antagonist candesartan on the dysregulation of AQPs and key renal sodium transporters in rats subjected to 24-h BUO and followed 2 days after release of BUO (BUO-2R). Consistent with previous observations, BUO-2R resulted in a significantly decreased expression of AQP1, -2, and -3 compared with control rats. Concomitantly, the rats developed polyuria and reduced urine osmolality. Moreover, expression of the type 2 Na-phosphate cotransporter (NaPi-2) and type 1 bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) was markedly reduced, consistent with postobstructive natriuresis. Candesartan treatment from the onset of obstruction attenuated the reduction in GFR (3.1 +/- 0.4 vs. 1.7 +/- 0.3 ml.min(-1).kg(-1)) and partially prevented the reduction in the expression of AQP2 (66 +/- 21 vs. 13 +/- 2%, n = 7; P < 0.05), NaPi-2 (84 +/- 6 vs. 57 +/- 10%, n = 7; P < 0.05), and NKCC2 (89 +/- 12 vs. 46% +/- 11, n = 7; P < 0.05). Consistent with this, candesartan treatment attenuated the increase in urine output (58 +/- 4 vs. 97 +/- 5 microl.min(-1).kg(-1), n = 7; P < 0.01) and the reduction in sodium reabsorption (433 +/- 62 vs. 233 +/- 45 micromol.min(-1).kg(-1), n = 7; P < 0.05) normally found in rats subjected to BUO. Moreover, candesartan treatment attenuated induction of cyclooxygenase 2 (COX-2) expression in the inner medulla, suggesting that COX-2 induction in response to obstruction is regulated by ANG II. In conclusion, candesartan prevents dysregulation of AQP2, sodium transporters, and development of polyuria seen in BUO. This strongly supports the view that candesartan protects kidney function in response to urinary tract obstruction.
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PMID:Angiotensin II mediates downregulation of aquaporin water channels and key renal sodium transporters in response to urinary tract obstruction. 1675 30


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