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)

Primary vesicoureteral reflux was seen in 2 siblings in a family of 5 (1 daughter and 2 sons). Voiding cystogram of elder sister, who complained of fever and backache, showed bilateral reflux at the age of 6. Left reflux disappeared soon but right reflux persisted. Right antireflux operation was performed at the age of 9, but right renal function deteriorated gradually. Right nephrectomy was done at the age of 12 because of persistent pyuria and renal stones. The second case was her younger brother who was sent to us because of proteinuria and hypertension. Excretory urogram showed left small kidney and voiding cystogram showed bilateral reflux with moderately dilated ureter and calyceal blunting. Urinalysis revealed normal findings except for proteinuria and he had no urological symptoms. Renal angiogram and renal vein renin study were unremarkable, so bilateral antireflux operation was done. Findings of urinalysis of his parents and younger brother were normal and cystogram of his brother was normal.
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PMID:[Familial vesicoureteral reflux]. 667 4

Unilateral uareteral obstruction (UUO) in 6-week old male spontaneously hypertensive rats (6-w-SHR) accelerated the elevation of blood pressure and developed stroke with high frequency from 3 weeks after operation, whereas UUO had no effect in either 20-week old SHR or 6-week old normotensive Wistar Kyoto rats. Urinary protein excretion and plasma urea and renin concentrations in 6-w-SHR began to increase 2 weeks after UUO. Removal of the obstructed kidney in 6-w-SHR one week after UUO prevented the acceleration of hypertension, while the same treatment 2 weeks after operation did not. In the ureter-obstructed kidneys of 6-w-SHR, hydronephrotic atrophy was markedly observed already one week after operation, while in the opposite kidneys, hypertensive vascular lesions were manifested from the second week. These results indicate that with regard to reversibility of the hypertensive process, the obstructed kidney is more important in the early postoperative stages and the contralateral kidney more important later.
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PMID:Acceleration of hypotension and development of stroke in the spontaneously hypertensive rat by unilateral ureteral obstruction. 699 78

The case is reported of a young woman with severe hypertension, unilateral renal artery stenosis, variously normal or marginally high plasma concentrations of active renin, angiotensin II, aldosterone, sodium, and potassium; and normal total exchangeable and total body sodium and potassium. Arteriograms and ureter catheterization showed the stenosis to be severe, but the unstimulated renal vein renin and angiotensin II differential to be modest. Captopril caused an initial fall in angiotensin II and arterial pressure. During prolonged captopril treatment, plasma angiotensin II and aldosterone remained depressed; exchangeable and total body sodium and potassium were unaltered. Blood pressure fell further to normal levels during prolonged captopril treatment, while subsequent surgical correction of the renal artery stenosis was curative; absolute values of blood pressure and plasma angiotensin II were similar in both situations. The findings support, without proving, the concept that chronic modest elevation of angiotensin II may be responsible for sustained hypertension in unilateral renal artery stenosis. Patients of this type contrast sharply with those, also with severe renal artery stenosis or occlusion, who have gross elevation of renin, angiotensin II, and aldosterone, with sodium and potassium deficiency. Captopril or surgery are effective in both syndromes, but the manner of response to treatment differs markedly.
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PMID:Renal artery stenosis with normal angiotensin II values. Relationship between angiotensin II and body sodium and potassium on correction of hypertension by captopril and subsequent surgery. 700 27

The mechanism whereby renal nerves influence the renin-release response to aortic constriction was examined in a nonfiltering ureter-occluded kidney preparation in anesthetized dogs. The kidney was rendered nonfiltering by a combination of mannitol infusion and ureteral occlusion. Suprarenal aortic constriction reduced renal perfusion pressure to 61 +/- 7 mmHg and increased renin release from 16.7 +/- 4.1 to 26.1 +/- 6.0 U/min. At normal renal perfusion pressure, low-frequency renal nerve stimulation (0.25 Hz) increased renin release by 11.6 +/- 4.2 to 25.1 +/- 7.6 U/min. The effect of combined low-level renal nerve stimulation and aortic constriction on renin release was additive; renin release increased by 24.6 +/- 6.5 to 39.5 +/- 7.3 U/min. Propranolol or metoprolol, administered intrarenally at 2 microgram . min-1 . kg-1, abolished the renin-release response to low-level renal nerve stimulation at normal renal perfusion pressure. These data provide evidence that low-frequency renal nerve stimulation influences the renin-release response to reduction in renal perfusion pressure in a nonfiltering ureter-occluded kidney with an inoperative macula densa receptor mechanism. The neural effect on renin release at normal renal perfusion pressure is mediated via beta 1-adrenoceptors probably located on the juxtaglomerular granular cells.
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PMID:Effect of low-level renal nerve stimulation on renin release from nonfiltering kidneys. 702 49

In ureter-ligated rats, the pressor effects of both norepinephrine and angiotensin II i.v. on systemic blood pressure and serum sodium concentration were significantly decreased when compared with those in control rats, while serum potassium concentration, blood urea nitrogen, mean systemic blood pressure and plasma renin activity were significantly increased. The microscopic examination of aortic smooth muscles did not show significant histological lesions in the tissues obtained from ureter-ligated rat. The responsiveness of aortic strips isolated from ureter-ligated rats to norepinephrine and angiotensin II was significantly decreased in comparison with that from control rats. The results suggest that a decreased pressor response to norepinephrine and angiotensin II under ureter-ligated conditions may be attributed to a decrease in vascular reactivity to drugs.
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PMID:Changes in vascular reactivity in rats with experimental renal insufficiency. 732 63

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

Haemodynamic changes in partial unilateral ureteric obstruction (PUUO) may be related to altered prostaglandin synthesis. In 12 dogs the left ureter was partially obstructed for 5 weeks. In six dogs the ureter was reimplanted into the bladder and to investigate the effect of this procedure on the contralateral side the other six animals underwent ipsilateral nephroureterectomy. Renal blood flow (RBF) was measured by the distribution of radiolabelled microspheres. Changes in urinary prostaglandin (PG) concentrations were validated by renin activity using angiotensin I. Reduced left RBF during obstruction was associated with increased thromboxane A2 synthesis (P < 0.01). Increased RBF to the non-obstructed side was associated with elevated PGE2 formation (P < 0.05). Elevated angiotensin I levels (P < 0.01) corresponded to maximal increases in PG synthesis. Reimplantation of the obstructed kidney did not exert a direct effect on contralateral RBF or PG concentration. Haemodynamic changes in PUUO in vivo are associated with alterations in renal PGs.
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PMID:Renal haemodynamics and prostaglandin synthesis in partial unilateral ureteric obstruction. 787 12

Acute unilateral ureteral obstruction (AUUO) has been associated to a blood pressure increase, presumably secondary to activation of the renin-angiotensin system (RAS), since the obstructed kidney increases renin secretion (Ref. 8). In an attempt to delineate the role of the RAS in this hypertensive model, we acutely obstructed the ureter in two groups of dogs that previous to the obstruction received either placebo (G I, n = 8) or 50 mg of captopril, an angiotensin-converting enzyme inhibitor (G II, n = 9). Animals that received placebo showed a consistent increase in mean arterial pressure (MAP), 128 +/- 4 vs. 144 +/- 4 mm Hg (p < 0.001); those that received captopril did not show such a tendency: 135 +/- 7 vs. 135 +/- 7 mm Hg. In further studies, three groups of animals were included: group III (G III, n = 4), identical to G I except that plasma renin activity (PRA) and aldosterone (ALDO) were measured; Group IV (G IV, n = 5), identical to G II except that they received 50 mg of indomethacin, 60 min before captopril; and group V (G V, n = 6), which was sham operated and measured for PRA and ALDO.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of the renin-angiotensin system in arterial hypertension secondary to acute unilateral urinary obstruction. 789 78

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

The secretion and synthesis of renin were studied in mice by measuring aortic, right and left renal vein renin, renal renin, and mRNA for renin. The role of the macula densa was evaluated in a kidney made hydronephrotic by tying the ureter 6 weeks earlier. There was no net secretion of renin from the left hydronephrotic kidney even when the mice were placed in a high secretory state by sodium restriction or enalapril. Sodium restriction and enalapril increased renin content to a similar extent in the normal and hydronephrotic kidney. High sodium intake decreased renin content in the normal and hydronephrotic kidney and also decreased the enalapril-stimulated renin content. Changes in mRNA in the same direction to renal renin implied that this was due to increased synthesis. Thus secretion and synthesis of renin can be disassociated. The macula densa is important for renin secretion but not for the stimulation of synthesis.
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PMID:Role of the macula densa in renin synthesis and secretion. 806 May 79


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