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)

A patient who presented with hypertension of recent onset was found to have unilateral hydronephrosis. Increased activity of the renin-angiotensin system was documented with renal-vein-renin concentrations. The hydronephrosis was due to a primary transitional cell carcinoma of the ureter. Following nephroureterectomy, blood pressure returned to normal and has remained so for two years.
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PMID:Reversible hypertension due to carcinoma of the ureter. 42 76

Uninephrectomized ewes were prepared with a renal artery flow probe and catheters were implanted into the renal artery, vein, and ureter. The renal perfusion pressure (RPP) of conscious animals was decreased externally by 13 +/- 3, 21 +/- 3, 31 +/- 3 mmHg over 5 min and returned to control levels over 5 min. Reduction of RPP by 13 and 21 mmHg resulted in prompt increases in renin secretion (RS) which were maximal coincident with the nadir of the downward ramp (delta RS 195 +/- 43 P less than 0.05, and 1,077 +/- 208 ng AI/min, P less than 0.01, respectively). Directly measured renal blood flow (RBF) was not decreased and no measurable change occured in GFR. When RPP was reduced by 31 mmHg, RBF and GFR were decreased and renin secretion rose further (delta RS 1,480 +/- 384 AI/min, P less than 0.05). On the upward pressure ramp, RS fell promptly and was nearly at control levels upon restoration of RPP. It was concluded that renin secretion responds rapidly to alterations in RPP in the autoregulatory range and these changes in renin secretion are unlikely to be mediated by a tubular receptor.
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PMID:Renin secretion during dynamic changes in renal perfusion pressure. 44 36

In anuric dogs loaded with K by infusion with 2 meq KCl/kg per h until prelethal hyperkalemic cardiotoxicity appears, the extent of transmembrane K transfer depends on the origin of the anuria. Animals with bilateral ureter ligation transfer a mean of 1.2 meq/kg to intracellular fluid, while those with bilateral nephrectomy transfer more than 2.5 times as much (3.1 meq/kg). Further, if dogs with functioning kidneys are ureter ligated or nephrectomized after approximately 45 min of K loading, K transfer ultimately falls as infusion continues. The fall is precipitate and over 90% in ligated animals; but it is gradual, and only 10% in those that are nephrectomized. Finally, K transfer, because of the absence of insulin, is negligible in K-loaded pancreatectomized dogs with bilateral ureter ligation, but fairly substantial in pancreatectomized animals with bilateral nephrectomy. The data suggest that ureter ligation and hyperkalemia activate a renal mechanism that interferes with the transfer of infused K to intracellular fluid. The mechanism may involve the renin-angiotensin II-aldosterone system to a limited degree.
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PMID:Inhibition of transmembrane K transfer in ureter-ligated dogs infused with KCl. 99 Jan 4

The purpose of this study is to demonstrate the developmental changes of the experimental hydronephrotic kidney using immunohistochemical, histoplanimetrical, and Northern blot techniques. At 1 month after ligation of the ureter, a large number of renin-positive cells were detected immunohistochemically even at a dilution of 1:10,000 in this hydronephrotic kidney; however, there were few renin-positive cells in the non-ligated side. At 6 months after ligation, no difference in reactivity for renin between ligated and non-ligated kidneys was demonstrated. In the morphometrical analysis of the renin-positive region, the numerical value of the ligated side was already increased at 2 weeks, reached the highest value at 1 month, and then decreased gradually to almost the same value as the control kidney by the end of the experiment. On the other hand, the value of the non-ligated side decreased immediately after the unilateral ligation, increased later, and finally reached almost the same value as the control kidney. In the Northern blot analysis, the activity of renin mRNA in the ligated side at 1 month after ligation was markedly higher than that in the non-ligated side. However, the difference between the ligated and the non-ligated sides was not demonstrated at 6 months and the value came to be almost the same as in the non-operated kidney.
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PMID:Morphological and northern blot analysis of juxtaglomerular cells in experimental hydronephrotic mice. 154 64

To examine whether autoregulatory dilation of preglomerular vessels enhances prostaglandin (PG)E2 and renin release during arachidonic acid infusion, the ureter was occluded or the renal artery constricted in anesthetized dogs. Intrarenal arachidonic acid infusion (40 micrograms X kg-1 X min-1) increased PGE2 release by 41 +/- 17 pmol/min at control pressures and by 149 +/- 60 pmol/min during ureteral occlusion. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) increased PGE2 release by 149 +/- 60 pmol/min at control pressures, by 505 +/- 211 pmol/min during ureteral occlusion and by 581 +/- 201 pmol/min during renal arterial constriction. Thus, PGE2 release during arachidonic acid infusion was trebled by autoregulatory dilation. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) raised renin release by 6 +/- 2 micrograms of angiotensin I per min at control pressures, by 25 +/- 9 micrograms of angiotensin I per min during renal arterial constriction and during ureteral occlusion by 16 +/- 4 micrograms of angiotensin I per min, which was not significantly higher than induced by the lower rate of infusion. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) raised renal blood flow by 54 +/- 5% at control pressures but exerted no vasoactive effect during ureteral occlusion and renal arterial constriction. We conclude that autoregulatory dilation enhances the stimulatory effects of arachidonic acid on renal PG synthesis. Both increased intrarenal PG concentration and autoregulatory dilation may contribute to enhancement of renin release. The stimulatory effects of arachidonic acid on PG synthesis and renin release are independent of the vasoactive effects of arachidonic acid.
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PMID:Autoregulatory vasodilation enhances renal prostaglandin E2 and associated renin release during arachidonic acid infusion in dogs. 392 29

We report a case of renal hypertension 6 months after a panhysterectomy for cervical cancer. Clinical investigation revealed that recurrent cancer obstructed the left ureter, resulting in the formation of a gigantic perirenal pseudocyst and, subsequently, hypertension. Constriction of the renal parenchyma was responsible for the overactivity of the renin-angiotensin system (the Page phenomenon). Ultrasound-guided percutaneous drainage relieved the symptomatology completely.
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PMID:Renal hypertension secondary to perirenal pseudocyst: resolution by percutaneous drainage. 405 80

Ethacrynic acid, a potent inhibitor of sodium reabsorption in the ascending limb of Henle's loop, produces a sharp rise in renal venous renin activity within 5 min after intravenous administration in anesthetized dogs. This response persists when volume depletion is prevented by returning urinary outflow to the femoral vein. Comparable studies with chlorothiazide, a diuretic with little or no effect on the medullary portion of the ascending limb of the loop of Henle, failed to produce a significant increase in renal venous renin activity.When administered during ureteral occlusion, ethacrynic acid produced no change in renal venous renin activity until ureteral occlusion was released and flow restored. Following release of the ureters, a prompt rise in renal venous renin was again observed within 5 min of release. Control studies of ureteral occlusion yielded a fall in renal venous renin activity following release of the ureter without administration of ethacrynic acid. These studies identify a prompt stimulatory effect of ethacrynic acid on renin release that is unrelated to volume depletion but dependent upon the presence of tubular urine flow. Although further definition of the site and characteristics of the distal tubular mechanism for stimulation of renin release requires more direct study, the data presented here indicate that changes in sodium concentration in distal tubular fluid serve as a stimulus for renin release.
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PMID:The effect of altered sodium concentration in the distal nephron segments on renin release. 431 94

These experiments were designed to study the role of calcium in the modulation of renin secretion by alpha and beta adrenoceptors. Rabbit kidneys were isolated and single-pass perfused with a modified Ringer's solution. Renal perfusion pressure was precisely controlled by an electronic servocontrol system. Tubular events were minimized by ligation of the ureter before initiating the studies. Under these conditions the predominant factor modifying renin secretion was assumed to originate directly on the juxtaglomerular cells. Isoproterenol infused at 0.1, 0.5, 1.0 and 5.0 nM/min/g of kidney weight increased renin secretion in a dose-dependent manner whereas phenylephrine infused at identical molar doses did not. In addition, phenylephrine (5.0 nM/min/g of kidney weight) blocked the usual response to isoproterenol. Removal of calcium from the perfusing medium had no effect on either the response to isoproterenol or the lack of a response to phenylephrine. On the other hand, when calcium is removed from the perfusate or when D-600, a calcium channel blocker, is added to calcium-containing medium, phenylephrine failed to block the usual response to isoproterenol. We conclude that the suppression of beta adrenoceptor stimulation of renin release by alpha adrenoceptor agonists is calcium dependent by a final mechanism as yet undefined, but probably involving movement of calcium into the juxtaglomerular cells.
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PMID:Role of calcium in the interaction of alpha and beta adrenoceptor-mediated renin release in isolated, constant pressure perfused rabbit kidneys. 631 14

This study tested the ability of the converting enzyme inhibitor, captopril, to lessen the severity of acute renal failure following temporary occlusion of the renal artery. In the control group, 11 dogs were anesthetized with halothane, and the left kidney was isolated through a midline incision. The renal artery, vein, and ureter were then clamped for 120 min. Immediately after occlusion, the kidney was flushed with 40 ml of saline at 34 degrees C. When the clamp was released, a contralateral nephrectomy was performed and the animal allowed to recover. Serum creatinine and blood urea nitrogen levels were followed on a daily basis thereafter. Thirteen captopril-treated dogs were treated in the same fashion except that captopril (1.25 ml/kg, i.v.) was given prior to the 120-min period of renal ischemia. Three of 11 (27%) control dogs survived, whereas 10 of 13 (77%) captopril-treated animals survived (P less than 0.05). Serum creatinine (5.4 +/- 2.5 mg/dl) and serum urea nitrogen (96 +/- 33 mg/dl) peaked on day 8 in the captopril-treated group and were consistently lower than in the untreated group. These observations suggest that captopril is useful when temporary interruption of the renal circulation is encountered, such as in renal autotransplantation, cadaveric renal transplantation, and renal revascularization. These data also suggest that inhibition of the renin-angiotensin system may lessen the severity of acute renal failure following renal ischemia.
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PMID:Enhancement of recovery in postischemic acute renal failure with captopril. 637 20

To study the relationship between PGE2 and renin release from the kidney, examinations were performed on anesthetized dogs during afferent arteriolar dilation. This condition is known to increase renin release and enhance the stimulatory effects on renin release of beta-adrenergic agonists, such as isoproterenol. Afferent arteriolar dilation induced by constricting the renal artery or occluding the ureter increased PGE2 and renin release before, but not after, indomethacin administration. Isoproterenol infusion during afferent arteriolar dilation increased renin release but not PGE2 release both before and after indomethacin administration. Phenylephrine, an alpha-adrenergic agonist, which also induces afferent arteriolar dilation, increased PGE2 and renin release at control blood pressure but not when the afferent arterioles already were dilated by ureteral occlusion. We conclude that afferent arteriolar dilation caused by renal arterial constriction, ureteral occlusion or infusion of phenylephrine increases prostaglandin synthesis which stimulates renin release. The effect of isoproterenol on renin release is independent of prostaglandin synthesis.
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PMID:Relationship between PGE2 and renin release in dog kidneys. Effects of afferent arteriolar dilation and adrenergic stimulation. 638 24


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