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)

We compared the effect of the renal nerves on renal function, plasma renin activity, and renal renin and angiotensinogen mRNA contents in Wistar rats and spontaneously hypertensive rats (SHR). Rats were anesthetized with sodium pentobarbital, the left kidney was exposed, its nerves were sectioned, the ureter was cannulated, and a flow probe was placed on the renal artery. The renal nerves were stimulated for 1 hour to reduce renal blood flow by 15% and 30%, after which blood was removed for measurement of plasma renin activity, and kidneys were analyzed for renal renin and angiotensinogen mRNA. Frequency-related reductions in filtration rate were similar, from 15% to 50%, as was sodium excretion, from 30% to 70%, in both SHR and Wistar rats. Basal plasma renin activity and responses to nerve stimulation in SHR were approximately half those of Wistar rats (all P < .001). SHR renal renin mRNA concentrations were approximately three quarters those of Wistar rats and were unchanged by either low- or high-level renal nerve stimulation, whereas the higher rate increased renin mRNA approximately threefold (P < .05) in the Wistar rats. SHR renal angiotensinogen mRNA was one quarter that of the Wistar rats and was unaffected by nerve stimulation, whereas in the Wistar rats it was increased threefold (P < .05) by the low but not high level of nerve stimulation. These findings show that whereas the renal nerves are able to modulate hemodynamic and tubular functions relatively normally in SHR, their ability to increase renin release, renal renin, and angiotensinogen mRNA levels is depressed.
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PMID:Renal nerves, renin, and angiotensinogen gene expression in spontaneously hypertensive rats. 772 1

We have shown that acute (24-hr) unilateral ureteral obstruction (UUO) induces the genes encoding for renin, in juxtaglomerular apparatuses and in tubules, for angiotensin converting enzyme in vascular endothelial cells, and for angiotensinogen in perivascular fat. These molecular changes occur in temporal association to marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR), suggesting that angiotensin II (Ang II) is at least partly responsible for the renal vasoconstriction. We tested the hypothesis that down-regulation of the Ang II type-1 receptor (AT1-R) gene occurs in UUO in response to Ang II, by examining the effects of an ACE inhibitor [lisinopril (Li), 5 mg/kg/day] and of the specific nonpeptidic AT1-R blocker, losartan (Lo) (10 mg/kg/day). UUO or sham operated (which included manipulation but not obstruction of the ureter) rats (S) were studied. Northern blot analysis of the steady state concentration of AT1-R mRNA corrected for GAPDH mRNA showed a marked decrease in receptor expression (-77%, N = 4, P < 0.01) in the obstructed kidney (UUO) compared to S; sham diminished gene expression modestly compared to the contralateral kidneys (C) of UUO. In situ hybridization for AT1-R mRNA also showed diminished expression in UUO compared to C kidneys (N = 4). Treatment of UUO rats (N = 4) with Lo increased AT1-R mRNA five times above the levels in UUO rats receiving vehicle; the increase induced by Li was 50% that of Lo; S (N = 4) and C (N = 4) did not change. Losartan, but not vehicle treatment increased RBF (sixfold) and GFR (fivefold) in the UUO kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the renal angiotensin II receptor gene in acute unilateral ureteral obstruction. 793 8