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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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. Previous studies have established a marked difference in sensitivity to organic calcium channel blockers of the phasic compared with tonic component of the contraction to potassium chloride (KCl) in the guinea-pig ureter. The mechanisms responsible for this difference have remained unsettled. In particular, the possible involvement of non-L-type calcium channels in contractility of the ureter has not been determined. In this study we have re-addressed this problem and, to eliminate any possible contribution of sensory neuropeptides released by KCl from peripheral endings of afferent nerves, all experiments were performed in ureters pre-exposed to the sensory neurone blocking agent, capsaicin (10 microM for 15 min). 2. Increasing concentrations of KCl (10-160 mM) produced phasic and tonic contractions of the guinea-pig isolated ureter: the L-type calcium channel agonist, Bay K 8644 (1 microM), enhanced both components of the contraction to KCl. 3. Nifedipine (1 microM) abolished all responses to increasing concentrations of KCl after 60 min contact time; after a shorter incubation period (15 min), the phasic contractions to low KCl concentrations were still observed, while the tonic responses were abolished. 4. The effects of nifedipine (0.1 nM-1 microM) on the phasic and tonic components of the response to 80 nM KCl were assessed after 15-120 min contact time. Nifedipine was equipotent in inhibiting the tonic response at all times tested, while a marked time-dependency of inhibition toward phasic responses was observed. After 15 min contact time, nifedipine was 181 times more potent in inhibiting tonic than phasic response to KCl, while after 120 min contact time the difference between EC50 values was only 5.4 times. 5. Cadmium chloride (3-30 microM) was equi-effective in inhibiting the phasic and tonic responses to KCl while nickel chloride was ineffective at 10-fold higher concentrations. omega-Conotoxin (0.1 microM) and tetrodotoxin (0.3 microM) were ineffective. 6. The present findings indicate that L-type voltage-dependent calcium channels mediate both phasic and tonic components of the response of the guinea-pig ureter to KCl while neither T-type nor N-type voltage-dependent calcium channels are involved. The marked time-dependency of inhibitory action of nifedipine suggests that L-type voltage-dependent calcium channels which are responsible for the generation of phasic contraction of the ureter are in a low affinity state for interaction with nifedipine.
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PMID:A pharmacological analysis of calcium channels involved in phasic and tonic responses of the guinea-pig ureter to high potassium. 753 37

Kidney function of the euryhaline toad Bufo viridis was studied in animals acclimated to tap water and solutions of NaCl (230 and 500 mosmol.kg-1 H2O) and urea (500 mmol.l-1) in steady-state conditions. An ureter was catheterized for continuous urine collection and blood was sampled from an iliac artery. A single injection of 3H-inulin served for estimation of glomerular filtration rate: this was in the range of 15-27 ml.kg-1.h-1 and did not differ significantly in any of the acclimation conditions. Urine flow, on the other hand, varied considerably and was highest in tap water (18.2 +/- 3.2 ml.kg-1.h-1; urine/plasma inulin ratio = 0.88), lower in 230 mosmol.kg-1 H2O NaCl solution (13.5 +/- 3.9 ml.kg-1.h-1; u/p inulin ratio = 1.73) and lowest in 500 mosmol.kg-1 H2O NaCl or urea acclimation solutions (5-7 ml.kg-1.h-1; u/p inulin = 3.7-4.2). Clearance of free water was high in the tap water group, lower in 230 mosmol.kg-1 H2O NaCl solution, and much lower in the hyperosmotic acclimation conditions. Clearances of both Na+ and Cl- were similar under our experimental conditions, but changed independently in accordance to the composition of the acclimation solution. Potassium clearance was similar in all acclimation conditions, and a constant plasma K+ concentration was maintained. Urea clearance was high in tap water and 500 mmol.l-1 urea acclimation groups and low in the NaCl acclimations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function at steady state in a toad (Bufo viridis) acclimated in hyperosmotic NaCl and urea solutions. 773 33

A 39-year-old male presented with gross hematuria and left lower abdominal discomfort. Excretory urography showed a left ureteral stone and hydronephrosis. CT scans and magnetic resonance imaging showed a solid mass at the upper pole of the left kidney. Angiography revealed a hypervascular lesion at this area. The laboratory data showed a slightly decreased serum potassium level. In the endocrinological study, the serum deoxycorticosterone (DOC) level was markedly elevated. There was, however, no evidence of hypertension. The operation was performed on November 13, 1992. The tumor was almost separated from the left kidney, but an aberrant artery which divided from the renal artery and penetrated the renal parenchyma was found. Therefore, we had to carry out en bloc removal of the tumor together with the left kidney and the ureter which contained the ureteral stone. Pathological diagnosis was adrenocortical carcinoma. After the operation, hypokalemia and the serum concentration of DOC returned to normal range. Therefore, the tumor was diagnosed as DOC producing adrenocortical carcinoma. The patient was discharged 30 days after the operation with uneventful postoperative course. He received 2.5 g of op'-DDD a day. There was no evidence of distant metastasis or local recurrence 12 months after the operation. Nineteen cases of DOC producing adrenocortical tumor have been reported in the world literature. A case and a review of the literature are herein reported.
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PMID:[Deoxycorticosterone-producing adrenocortical carcinoma--a case report]. 777 67

1. In single sucrose gap, electrical field stimulation (EFS, 1-5 Hz) produced graded hyperpolarization of the membrane of the guinea-pig ureter smooth muscle, which was blocked by tetrodotoxin (0.3 microM) or in vitro capsaicin desensitization (3 microM for 15 min). Capsaicin itself produced a transient hyperpolarization of the membrane on its first application. 2. Superfusion with human alpha calcitonin gene-related peptide (CGRP, 30-300 mM) likewise produced a transient hyperpolarization of the membrane, mimicking the neurogenic inhibitory junction potential (i.j.p.). The hyperpolarization by CGRP was unaffected by tetrodotoxin, indicating a postjunctional site of action. 3. Both the EFS-evoked i.j.p. and the CGRP-induced hyperpolarization were inhibited by the CGRP receptor antagonist, CGRP(8-37) (0.3-3 microM) which did not affect the hyperpolarization produced by the KATP channel opener, cromakalim (0.3 microM). 4. The KATP channel blocker, glibenclamide (1 microM) blocked both the EFS-evoked i.j.p. and the CGRP-induced hyperpolarization. 5. When evoked in a low K medium (1.2 mM, KCl being replaced by an equimolar amount of NaCl), the EFS-evoked i.j.p. and the CGRP-induced hyperpolarization were both markedly enhanced, consistent with the idea that opening of K channels underlies both responses. 6. The present findings provide direct electrophysiological evidence for a neurotransmitter role of CGRP, released from the peripheral endings of capsaicin-sensitive primary afferent neurones, in the guinea-pig ureter. The action of both exogenous and endogenous CGRP involves the activation of glibenclamide-sensitive (KATP) potassium channels.
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PMID:Inhibitory transmitter action of calcitonin gene-related peptide in guinea-pig ureter via activation of glibenclamide-sensitive K channels. 783 12

We have investigated the ability of human alpha CGRP (CGRP) to inhibit the electrically-evoked myogenic contractions of the guinea-pig ureter, in comparison with the K channel opener, cromakalim, and the adenylate cyclase activator, forskolin. CGRP (0.1 nM-0.1 microM) produced a concentration-dependent inhibition of the evoked contractions; its action was prevented by the CGRP receptor antagonist, CGRP(8-37) (1 microM), while it was unaffected by the nitric oxide (NO) synthase inhibitor, L-nitroarginine (30 microM). The effect of CGRP was antagonized in a noncompetitive manner (depression of Emax, no change in EC50) by glibenclamide (1-10 microM), a blocker of ATP-sensitive potassium channels (KATP). A substantial fraction of the inhibitory effect of CGRP was glibenclamide-resistant, however. Glibenclamide also blocked the inhibitory action of cromakalim (0.1-10 microM) without affecting the inhibition produced by forskolin (0.1-30 microM). When tested in a low-K medium (extracellular K reduced from 5.9 to 1.2 mM), the inhibitory effects of CGRP, cromakalim and forskolin were enhanced. The inhibitory effect of forskolin was partly antagonized by glibenclamide when tested in a low-K medium. CGRP (0.1 microM), cromakalim (3 microM) and forskolin (10 microM) inhibited the contractile response to KCl (80 mM), which is characterized by a distinct phasic and tonic component: cromakalim selectively inhibited the phasic response to KCl with CGRP and forskolin inhibited both components. The inhibitory effect of CGRP on the phasic contraction to KCl was partly glibenclamide-(1 microM) sensitive, while that on the tonic contraction was glibenclamide-resistant. The inhibitory action of forskolin on both components of the response to KCl was unchanged by glibenclamide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple mechanisms in the smooth muscle relaxant action of calcitonin gene-related peptide (CGRP) in the guinea-pig ureter. 787 Jan 93

1. We have investigated the effect of the potassium (K) channel opener, cromakalim, on the spontaneous myogenic activity of the guinea-pig isolated renal pelvis and on myogenic contractions evoked by direct electrical stimulation of the guinea-pig isolated ureter. 2. In the presence of Bay K 8644 (1 microM), electrical stimulation of the guinea-pig ureter (10 Hz for 1 s, pulse width 5 ms, 60 V) produced regular tetrodotoxin-(1 microM) resistant phasic contractions which were suppressed by 3 microM cromakalim. Glibenclamide (0.1-3 microM), 4-aminopyridine (4-AP, 0.1-2 mM) and tetraethylammonium (TEA, 1-10 mM) produced a concentration-dependent inhibition of the effect of cromakalim with the rank order of potency (EC50 in parentheses): glibenclamide (0.64 microM) >> 4-AP (1.11 mM) > TEA (6.6 mM). Apamin (0.1-0.3 microM) was without effect. 3. Cromakalim (0.1-10 microM) produced concentration-dependent inhibition and suppression of spontaneous contractions of the guinea-pig isolated renal pelvis and of evoked contractions of the ureter with EC50 values of 0.71 and 0.47 microM, respectively. 4. Glibenclamide (1 microM) produced a rightward shift of the concentration-response curve to cromakalim in both the renal pelvis and ureter, without producing depression of the maximal inhibitory effect. Glibenclamide did not affect the spontaneous activity of the renal pelvis while it produced a slight enhancement (10-15% increase) of evoked contractions of the ureter. Glibenclamide did not affect the inhibitory action of the adenylate cyclase activator, forskolin, in the renal pelvis or ureter. 5. In electrophysiological experiments (sucrose gap), cromakalim (0.3 and 1 microM) produced hyperpolarization of ureter smooth muscle. Cromakalim also produced a transient suppression of action potentials and accompanying phasic contractions evoked by electrical stimulation. Before suppression of evoked contractions, a shortening of action potential duration was observed concomitant with the developing hyperpolarization produced by cromakalim. A lower concentration (0.1 MicroM) of cromakalim did not affect membrane potential but shortened action potential duration and reduced the evoked contraction.6. Glibenclamide (1 MicroM) inhibited the hyperpolarizing action of cromakalim and prevented its inhibitory action on evoked action potentials and contractions of the ureter. Glibenclamide also produced a slight prolongation of action potential duration and increased the amplitude and duration of the accompanying mechanical response.7. These findings demonstrate that activation of cromakalim- and glibenclamide-sensitive K channels produces a powerful mechanism for regulation of pyeloureteral motility and suppression of latent pacemakers of the ureter in guinea-pig. Glibenclamide-sensitive K channels take part in determining action potential shape and duration in the guinea-pig ureter.
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PMID:Effect of cromakalim and glibenclamide on spontaneous and evoked motility of the guinea-pig isolated renal pelvis and ureter. 801 47

The requirements of organ cryopreservation differ from those of conventional organ preservation. The encouraging results of Karow's group with dog kidneys transplanted after perfusion with more than 4 M dimethyl sulfoxide were based on an RPS-2 (renal preservation solution 2) vehicle solution, but transplantation of rabbit kidneys after perfusion with RPS-2 has not been reported. We evaluated RPS-2 in comparison to Euro-Collins solution (EC) using a modified technique for rabbit kidney autotransplantation and a computer-based organ perfusion machine designed for the introduction and removal of cryoprotective agents. Consistent success in rabbit kidney transplantation was found to depend on the anesthetic used, the hydration volumes administered, and direct ureter-to-ureter anastomosis. RPS-2 was found to be equivalent to EC for short-term (about 5 h) preservation by either perfusion or simple cold storage. However, good results with EC were associated with perfusion at 4 degrees C, recovery being significantly worse at 2 degrees C. In addition, we found that the solitary rabbit kidney is not able to fully compensate for the loss of the contralateral kidney, the result being persistent (to 3 weeks) mild elevation of serum creatinine, potassium, and calcium and persistent moderate reduction of serum phosphate. These results establish perfusates, perfusion conditions, transplantation techniques, computer-based perfusion control techniques, and a general clinical baseline that are permissive of further direct experiments on cryoprotectant introduction and removal.
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PMID:Cryopreservation of the mammalian kidney. I. Transplantation of rabbit kidneys perfused with EC and RPS-2 at 2-4 degrees C. 815 95

1. Chronic hypoxic rats are always polycythaemic. It is possible that an increase in packed cell volume may enhance erythrocyte trapping with a consequent increase in renal damage after renal ischaemia. These experiments were designed to assess renal functional changes after renal arterial occlusion in chronic hypoxic rats. 2. Chronic hypoxic rats were prepared by exposure (15h/day) to an altitude chamber (5486m) for 4 weeks. 3. After 45 min of left renal arterial occlusion, there were significant decreases in the excretion of potassium, p-aminohippurate and inulin and in the p-aminohippurate extraction ratio in 12 sea level ischaemic insulted kidneys. In 12 chronic hypoxic rats, the same parameters were changed after left renal ischaemia but only the p-aminohippurate ratio was significantly altered. 4. Administrations of 1 or 5 mg/kg phosphoramidon did not cause any significant improvement in the measured renal parameters in both kidneys and in both groups of rats after ischaemia. 5. In the second experiment, the rats were challenged by rapid infusion of 10 ml of saline intravenously, and urine was collected for 90 min from each ureter. Four hours after left renal arterial occlusion, the insulted kidney showed increased water and sodium excretion in both sea level and chronic hypoxic rats. However, 24 h after left renal ischaemia, the responses of sea level and chronic hypoxic rats were different. Urinary excretion was significantly reduced in sea level rats, but was almost normal in chronic hypoxic rats. 6. This report suggests that some beneficial factors after chronic hypoxia might play important roles in reducing the damage after renal ischaemia.
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PMID:Renal functional response to ischaemic renal failure in chronic hypoxic rats. 840 80

A protective action of lasix, dichlothiazide, and triampur (dichlothiazide + triamterene) was studied in experiments on rats. Ischemia was simulated by obstruction of kidney vessels and ureter for 90 min. Lasix and dichlothiazide produced a protective effect in renal ischemia and at the same time resulted decrease of lifetime of experimental rats. Triampur increased the lifetime and decreased the losses of potassium in kidney tissue.
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PMID:[The action of diuretics in renal ischemia]. 870 84


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