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 case of diverticular stones in the male anterior urethra with retrocaval ureter is reported. A 26-year-old man visited our hospital for examination, who had experienced spontaneous stone discharge a few days earlier. Computed tomographic (CT) scan with ureteral catheterization and urethrography revealed a retrocaval ureter and urethral diverticular stones. Resection of urethral diverticulum with 7 stones and right ureteroplasty were performed. The urethrography and drip infusion pyelography (DIP) 9 months after operation showed no abnormal findings. The largest stone was 28 x 22 x 20 mm in size and 20 g in weight. The main components were ammonium dihydrogen-urate (70%), carbonate apatite and struvite. Histological feature of the epithelium of the urethral diverticulum indicated normal skin with hairs. Pathological diagnosis was para-urethral dermoid cyst. Our case is the 67th case of the male urethral diverticular stones and the first case of those with retrocaval ureter in Japan.
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PMID:[Anterior urethral diverticular stones and retrocaval ureter in male: a case report and review of literature in Japan]. 135 38

Factors affecting intracellular pH (pHi) in the smooth muscle of guinea pig ureter have been investigated using pH-sensitive microelectrodes. Associated acids and bases appear to have free passage across the cell membrane but results suggest very low permeability to charged acid equivalents, thus implicating carrier-mediated movements in many of the observed pHi transients. Recovery from acidosis in the nominal absence of CO2 was inhibited by removal of Na+ and by the presence of amiloride, indicating that Na+/H+ exchange was responsible. The presence of CO2 resulted in a faster recovery from acidosis but, since intracellular buffering power was not increased, not a substantially faster effective extrusion of protons. Surprisingly, amiloride no longer caused discernable inhibition. Recovery from moderate acidosis remained Na+ dependent but was not inhibited by DIDS or acetazolamide or by the absence of Cl-, suggesting a dominant Na+-, and HCO3(-)-dependent mechanism unlike any hitherto described. Recovery from alkalosis was inhibited by DIDS and Cl(-)-free conditions, indicating that Cl-/HCO3- exchange was involved. Results suggest reversal of this mechanism on extreme acidosis. Experiments in vascular smooth muscle with fluorescent indicators confirm the presence of Na+/H+ exchange but provide conflicting evidence about the presence and properties of the HCO3(-)-dependent mechanism.
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PMID:Movement of acid equivalents across the mammalian smooth muscle cell membrane. 284 29

The ultrastructural localization of carbonic anhydrase (CA) was investigated with the cobalt-bicarbonate method in three epithelia of the pond snail Lymnaea stagnalis. In the epidermis a selective population of "positive cells" was observed. In these cells, CA is confined to the apical and to small parts of the lateral plasma membrane. In cells of the outer mantle epithelium, CA is localized in the lateral and basal parts of the plasma membrane. In cells of the ureter, CA was found apically as well as basally. The localization of CA is discussed in relation to the different functions of the epidermis (electrolyte uptake), mantle (HCO3- secretion, calcification) and ureter (electrolyte uptake, acid-base regulation).
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PMID:Ultrastructural localization of carbonic anhydrase in tissues involved in shell formation and ionic regulation in the pond snail Lymnaea stagnalis. 677 62

1. HCO3(-)-dependent mechanisms involved in the regulation of intracellular pH (pHi) were characterized using double-barrelled pH-sensitive microelectrodes in smooth muscle cells of the isolated guinea-pig ureter. 2. Removal of external Cl- in the presence of CO2-HCO3- caused a transient alkalosis, consistent with the presence of Cl(-)-HCO3- exchange, before pHi slowly recovered. Recovery from acidosis in the presence of CO2-HCO3- was not affected, at a time when intracellular Cl- would have been maximally depleted, indicating that a counter transport of Cl- and HCO3- was not involved. The recovery was also not affected by amiloride, indicating that Na(+)-H+ exchange was not involved. 3. A transient hyperpolarization was associated with the recovery from acidosis in the presence of CO2-HCO3-, consistent with rheogenic coupling of Na(+)-HCO3- cotransport. However, depolarization caused by elevation of the extracellular potassium (K+o) concentration, which should favour inward transport by the rheogenic mechanism, caused a fall in pHi and decreased the rate of recovery from acidosis. Furthermore, ouabain abolished the transient hyperpolarization without affecting the recovery of pHi. It is concluded that Na(+)-HCO3- cotransport in the ureter is electroneutral. 4. Recovery from acidosis in the presence of CO2-HCO3- was insensitive to DIDS even after prolonged pre-equilibriation and extreme acidosis. The results suggest that Na(+)-HCO3- cotransport in the ureter is insensitive to DIDS and that Cl(-)-HCO3- exchange does not reverse to contribute to the extrusion of acid equivalents. A HCO3- conductance may account for the Na(+)-independent, HCO3(-)-dependent recovery from extreme acidosis. 5. Recovery from experimentally induced alkalosis was inhibited by Cl(-)-free conditions and by DIDS, indicating that Cl(-)-HCO3- exchange was involved. 6. It is concluded that pHi in the smooth muscle of guinea-pig ureter is controlled by three transport mechanisms. By far the most important is an electroneutral Na(+)-HCO3- cotransporter. Na(+)-H+ exchange appears to play little role in the presence of the physiological buffer. Both of these mechanisms extrude acid equivalents and so protect the cell against its fairly substantial intrinsic intracellular acid loading. Cl(-)-HCO3- exchange, on the other hand, is stimulated by intracellular alkalosis to transport acid equivalents into the cell and so restore a more normal pHi.
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PMID:Regulation of intracellular pH in the smooth muscle of guinea-pig ureter: HCO3- dependence. 752 76

The luminal membrane of collecting duct cells, especially the intercalated cells, is normally exposed to active kallikrein. This is the consequence of the specific localization of this renal enzyme in the connecting tubule cells and its principal route of secretion being into the tubular lumen. It is conceivable that kallikrein acts downstream on a transporter involved in distal bicarbonate handling. To investigate this possibility, we estimated bicarbonate concentration and measured kallikrein amidolytic activity in urine fractions collected after a classical stop-flow experiment in rabbits. A highly significant inverse correlation was found between these parameters (r = -0.94, p < 0.001) in the peak kallikrein fractions. Neither sodium nor potassium concentration were correlated to kallikrein. This suggests that the physiological role of renal kallikrein may be to regulate extracellular fluid pH by inhibiting collecting duct bicarbonate secretion. To test the hypothesis that tubular fluid kallikrein activity and bicarbonate secretion are causally related, we developed a novel in vivo stop-flow injection model ('orthograde stop-flow'). A hog-kallikrein containing solution (0.5 microgram/ml) was injected through the abdominal aorta into the renal tubular system of one kidney of barbiturate-anesthetized rats, while the renal blood supply was interrupted. The ureter was then occluded and renal blood perfusion reinitiated. After a 2-min contact time five 125-microliters urine fractions were collected. Bicarbonate secretion was clearly detected in the second and third fractions (i.e. those coming from the collecting ducts) of the control animals, which had received only the vehicle. There was no bicarbonate secretion peak in the corresponding urine fractions collected from kallikrein-injected animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for an inhibitory effect of kallikrein on collecting duct bicarbonate secretion in rats and rabbits. 753 9

1. Mechanisms involved in the regulation of intracellular pH (pHi) in smooth muscle cells of guinea-pig ureter have been investigated using double-barrelled pH-sensitive microelectrodes in isolated strips of tissue. 2. Removal of CO2-HCO3- from the superfusing solution caused a fall in the steady-state pHi except in a few cells which had been excised from the animal for many hours (usually > 24 h). The pHi value was 7.22 +/- 0.09 (n = 89; mean +/- S.D. of an observation) in solution buffered with 5% CO2-21 mM HCO3-, compared with 6.92 +/- 0.24 (n = 67) in the nominal absence of CO2-HCO3-. Recovery from experimentally induced acidosis was faster in the presence, rather than nominal absence, of CO2-HCO3- (mean half-times of 2.7 +/- 0.7 min, n = 41, and 4.6 +/- 1.3 min, n = 12, respectively). These results suggest the presence of both HCO(3-)-dependent and -independent mechanisms for the effective extrusion of acid equivalents. 3. Recovery from acidosis was dependent on external Na+ (Na+o) in both the presence and nominal absence of CO2-HCO3-, with an apparent half-maximal activation at approximately 4 and 20 mM Na+o, respectively. Removal of Na+o in the steady state caused a fall in pHi which proceeded at a faster rate in the presence rather than in the nominal absence of CO2-HCO3-. 4. Amiloride (100 microM-1 mM) reversibly inhibited the recovery from acidosis and caused a fall in the steady-state pHi when applied in the nominal absence of CO2-HCO3-, but had no measurable effect on either the recovery from acidosis or steady-state pHi in the presence of CO2-HCO3-. These results suggest that Na(+)-H+ exchange was responsible for extrusion of acid equivalents in the nominal absence of CO2 and HCO3-, but that it played little part under more physiological conditions. 5. Although Na(+)-H+ exchange appeared to be activated below a pHi of about 7.2, it was incapable of maintaining a 'normal' pHi in the nominal absence of CO2-HCO3- in freshly excised cells, where values between 6.06 and 6.89 were recorded. Only in aged preparations, in which the intrinsic intracellular acid loading was substantially reduced (as judged from the rate of acidification on application of amiloride in the nominal absence of CO2-HCO3-) did the steady-state value approximate to that observed in the presence of CO2-HCO3-, at about 7.2.
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PMID:Regulation of intracellular pH in the smooth muscle of guinea-pig ureter: Na+ dependence. 779 29

1. Intracellular pH (pHi) of smooth muscle cells in isolated strips of guinea-pig femoral artery was measured using double-barrelled pH-sensitive microelectrodes. 2. In modified Krebs solution equilibrated with 5% CO2, pHi was 7.26 +/- 0.14 (n = 36; mean +/- S.D. of an observation) and the membrane potential (Em) was -60.5 +/- 5.5 mV. Removal of CO2 from the superfusing solution caused an immediate transient alkalosis before pHi stabilized at much the same value (7.28 +/- 0.14; n = 16) as in the presence of CO2. 3. The rate of recovery of pHi from experimentally induced acidosis was not measurably affected by the presence or nominal absence of CO2-HCO3-. 4. Application of amiloride (100 microM) blocked recovery from acidosis in the nominal absence of CO2-HCO3- and caused a progressive fall in pHi. In the presence of CO2-HCO3-, application of amiloride allowed a slow recovery to pHi 6.7-7.0, but completely prevented full recovery to the normal pHi. 5. Removal of extracellular Na+ (Na+o) caused a dramatic, progressive fall in pHi in both the presence and nominal absence of CO2-HCO3-. 6. The amiloride-insensitive extrusion of acid equivalents observed in the presence of CO2-HCO3- to pHi 6.7-7.0 was inhibited by removal of Na+o but was not affected by preequilibration with DIDS (see Methods). 7. It is concluded that Na(+)-H+ exchange is largely responsible for the effective extrusion of acid equivalents in these arterial cells, at least from relatively small perturbations. A DIDS-insensitive, Na(+)- and HCO3(-)-dependent mechanism provides some recovery from acidosis to a relatively low pHi. 8. Comparison with data obtained in exactly the same manner in smooth muscle cells of the guinea-pig ureter indicates that there are significant differences in the regulation of pHi in different smooth muscles.
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PMID:Regulation of intracellular pH in smooth muscle cells of the guinea-pig femoral artery. 779 30

We report a case of active tuberculosis associated with a right nonfunctioning kidney and nearly total loss of bladder capacity. Percutaneous nephrostomy and right nephroureterectomy were performed while the patient was undergoing triple drug therapy. Definitive surgical treatment consisted of ileal bladder augmentation and ileal ureter replacement. Normal urodynamics of the upper urinary tract and normal voiding with complete return of bladder capacity were achieved. Metabolic acidosis was treated successfully by sodium hydrogen carbonate.
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PMID:Ileal bladder augmentation combined with ileal ureter replacement in advanced urogenital tuberculosis. 815 83

1. We have altered intracellular (pHi) and extracellular pH (pHo) in the smooth muscle of guinea-pig ureter and determined the effects on evoked phasic contractions. In order to investigate the mechanisms underlying the effects of pH alteration, intracellular Ca2+ ([Ca2+]i), pHi, electrical activity and force were measured. 2. Intracellular acidification, produced by the weak acid butyrate, application of CO2 at constant pHo or removal of weak bases, greatly increased phasic contractions. Alkalinization with weak bases or by removal of CO2 inhibited contractions. The results were similar whether Hepes or CO2-HCO3-buffered the solutions. 3. Phasic contractions were preceded by intracellular Ca2+ transients in the ureter. Acidification of the cytoplasm led to an increase in the amplitude of the Ca2+ transient, and alkalinization decreased its magnitude. 4. In the ureter the action potential leads to Ca2+ influx, therefore electrophysiological recordings of its configuration were made during alteration of pHi. Acidification led to the action potential duration and amplitude being increased, whereas alkalinization shortened the action potential and reduced its amplitude. 5. As the effects of acidification on the action potential resembled the effects of blocking of K+ channels, we investigated whether pHi alteration was able to alter tension when K+ channels were blocked by tetraethylammonium. Acidification was unable to potentiate force under these conditions nor did alkalinization decrease force. 6. External pH over the range 6.8-8.0 had little or no effect on pHi, phasic contractions and [Ca2+]i. Tonic contractions were enhanced, however, when pHo was increased. 7. These data suggest that pHi alteration in the guinea-pig ureter modulates the action potential, probably by alteration of K+ currents. Subsequent changes in [Ca2+]i and contraction then occur. A potentiating effect of acidic pH on force is not common in muscle, but may be a characteristic of the smooth muscle of the urinary tract. Changes of pHo had little effect on phasic force or pHi, but modulated tonic contractions. The possible physiological significance of these results is discussed.
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PMID:An investigation into the mechanism whereby pH affects tension in guinea-pig ureteric smooth muscle. 879 6

A 5-year-old guinea pig was presented to the University of Berne Small Animal Radiology Department for an ultrasound examination of the abdomen to confirm a suspected diagnosis of Cushing's syndrome. The patient had bilateral alopecia, was apathic and obese. Ultrasonographically, a tumor of the left adrenal gland, obstruction of the left ureter by an ureterolith, as well as hydronephrosis of the left kidney were detected. During surgery to relieve the ureteral obstruction the adrenal gland tumor was removed. The guinea pig died post-operatively due to blood loss. The left adrenal gland tumor was found histopathologically to be an adenoma and the right adrenal gland also had multiple small adenomas, but grossly appeared normal. The ureterolith was analyzed and found by x-ray diffraction to consist of calcium carbonate.
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PMID:Ultrasonographic detection of adrenal gland tumor and ureterolithiasis in a guinea pig. 949 16


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