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

A partial obstruction of the left ureter was created in weanling (3-week-old) rats. Renal function was studied after 7-9 weeks and compared to that in age-matched controls. Arterial blood pressure was found substantially increased. During normal hydration, the hydronephrotic kidney had low excretions of urine, potassium, osmoles and, especially, sodium. The contralateral, intact side showed no compensatory traits. On volume expansion, the hydronephrotic kidney demonstrated an unimpaired reacting capacity, leading to normalization of urine, sodium and osmole excretions and even to supernormal renal blood flow, glomerular filtration and potassium excretion. On the intact side, the excretion of potassium was increased like that on the hydronephrotic one, while excretions of urine, sodium and osmoles were increased even more. The fact that the intact kidney handled most of the urine excretion was interpreted as the result of a mechanism protecting the obstructed kidney from additional pressure insults while homeostasis was maintained. The arterial hypertension may result from the combination of retention of fluid and sodium by the hydronephrotic kidney and the absence of compensation by the intact kidney during normal hydration--like that in everyday life. The functional changes during normal hydration were generally more severe than those we found after obstruction in neonatal and adult rats, in which arterial hypertension was never observed. The clinical implication would be that the kidney may be less tolerant to pressure rises during the infant year. Changes due to obstruction are known to occur rapidly, but after that neither progress nor reverse.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial ureteric obstruction in weanling rats. II. Long-term effects on renal function and arterial blood pressure. 141 99

Nowadays the postnatal management of antenatally detected hydronephrosis is much debated. Some authors claim that these cases ought to be operated very early, since there is rapid renal destruction and full recovery may only be achieved during this period. Others claim the opposite and recommend a nonoperative follow-up, provided that renal function is normal, as it is in the majority of cases. If experimental studies are to be used to settle this question, the created obstructions must correspond to human obstructions. That is, be partial and permanent, produced in fetal or newborn animals, preferably be moderate in degree, the diameter should grow in pace with the growing ureter, and be followed for a long period. Only three experimental series fulfil, to some extent, these requirements. In two of them a severe obstruction was produced, which within 5-8 weeks led to reductions by 80-95% in renal blood flow, glomerular filtration and potassium and phosphate excretions, which were in part compensated for and established early. In one study, a moderate obstruction was created which within 9 weeks led to reductions of 10-30% in renal blood flow, glomerular filtration, and potassium excretions, which were in part compensated for. The changes appeared very soon but were not progressive. Release of the obstruction had to be performed very early in order to avoid the lesions. The causes of the renal defects and of the absence of progression are discussed. It is concluded that the majority of human pyeloureteral obstructions are best imitated by a moderate type obstruction. The results do not support any rationale for early correction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suspected pyelo-ureteral junction obstruction in the fetus: when to do what? II. Experimental viewpoints. 202 16

A feasibility study has been carried out to evaluate rubidium-82, a potassium analog and generator-produced positron emitter, for measuring renal blood flow using a first pass model. Seven acute dogs were studied with beta probes and positron emission tomography to understand the dynamics of rubidium-82 in the kidneys. Preliminary results show that first pass extraction fraction for rubidium-82 ranged from 80-95% with an average of 89%. During the 150 sec of data collection, approximately 44.5% of the injected dose is excreted in the venous side and 9.75% in the ureter. Flow measurements with rubidium-82 and microspheres correlated well with the average control flow of 5.0 ml/min/gm measured by microspheres and 4.5 ml/min/gm of flow measured by rubidium-82 using the first pass model.
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PMID:Feasibility of measuring first pass extraction and flow with rubidium-82 in the kidneys. 209 Jan 64

Unheparinized, ureter-ligated control dogs that are potassium loaded, i.e., infused with 2 mEq of KCl/kg until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear (end point), transfer 57 +/- 4% (1.7 +/- 0.1 mEq/kg) of administered potassium to intracellular fluid. Heparinized controls transfer 73 +/- 1% (3.2 +/- 0.2 mEq/kg); with simultaneous alpha-adrenoreceptor blockade, that proportion increases to 81 +/- 2% (4.80 +/- 0.7 mEq/kg) and with simultaneous beta-receptor blockade it is 58 +/- 3% (1.1 +/- 0.1 mEq/kg). In potassium loaded, ureter-ligated dogs, heparin increases transmembrane potassium transfer as effectively as does a dosage of atropine large enough to cross the blood-brain barrier and its influence on potassium transfer, like that of atropine, is suppressed by beta-adrenoreceptor blockade.
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PMID:Heparin mediates transmembrane potassium transfer in hyperkalemic dogs. 223 6

The clinical usage of amphotericin B in treating systemic fungal infections is limited by its nephrotoxicity, which is caused by reductions in renal blood flow and alterations in renal tubular function. Aminophylline, an adenosine receptor antagonist, attenuates amphotericin B-induced reductions in renal blood flow in both dogs and rats, which suggests that endogenous adenosine may participate in this response. However, aminophylline per se is a vasodilator and also changes intracellular levels of cyclic nucleotides and calcium. In this study, we re-examined the hypothesis that adenosine participates in amphotericin B-induced renal vasoconstriction by employing a novel adenosine receptor antagonist, 1,3-dipropyl-8-(p-sulfophenyl)xanthine (DPSPX). This antagonist because of its negative charge at physiological pH, has limited access to the intracellular space. In a group of male Sprague-Dawley rats, an extracorporeal shunt was established between the carotid artery and left renal artery, via an aortic pouch, such that flow through the shunt was equivalent to renal blood flow. Also, a catheter was inserted into the left ureter for collection of urine and measurement of creatinine and electrolyte excretion. Amphotericin B-induced changes in renal blood flow and renal excretory function were measured in both control rats and rats pretreated with DPSPX at a dosage that abolishes the renovascular effects of exogenous adenosine in this model. In both control rats and rats pretreated with DPSPX, amphotericin B caused a marked decrease in renal blood flow, creatinine excretion, and potassium excretion; however, these effects of amphotericin B were similar in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of an adenosine receptor antagonist on acute amphotericin B nephrotoxicity. 234 Aug 62

The release of tachykinins from isolated slice preparations of the guinea-pig spinal cord and ureter was studied in vitro. Capsaicin (10 microM) caused release of substance P, neurokinin A and an eledoisin-like component from both the spinal cord and ureter. The release of tachykinins induced by capsaicin or potassium (60 mM) was calcium dependent. No detectable release of neurokinin B or neuropeptide K, an N-terminally extended form of neurokinin A, was induced by capsaicin. No detectable release of tachykinins could be demonstrated after exposure to agents which are known to activate C-fibre afferents, such as histamine, bradykinin, serotonin, prostaglandins E1, E2 or acetylcholine. Protein extravasation in the ureter, as determined by the Evans Blue extravasation technique was used as a functional correlate to the tachykinin release. Protein extravasation was induced in vivo by local intraluminal injections of capsaicin at several hundred-fold lower concentrations than those required to induce a detectable release of tachykinins in vitro. The difference may, however, partly depend on the experimental conditions and the detection limit of the tachykinin assay used. The protein extravasation response to capsaicin was absent after systemic capsaicin pretreatment, which causes a marked depletion of tachykinins in the ureter. In conclusion, capsaicin evokes release of several tachykinins from both central and peripheral endings of primary afferent neurons. The peptides released from sensory nerves in the periphery may induce effects such as protein extravasation and smooth muscle contraction.
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PMID:Capsaicin induced release of multiple tachykinins (substance P, neurokinin A and eledoisin-like material) from guinea-pig spinal cord and ureter. 243 50

The effects of caffeine on the electrical and mechanical activity of the guinea-pig ureter smooth muscle were studied. Under untreated conditions caffeine mainly showed inhibitory action on the ureter, inhibiting the evoked action potentials and phasic contractions as well as potassium contracture. Caffeine was also found to suppress the low-Na contracture of Na-loaded ureter muscle. It is established that Na-loaded tissue is able to generate transient contracture in response to caffeine application at 37 degrees C. These caffeine contractures could be evoked under completely removed [Ca2+]0 and in the presence of high doses of Ca-channel blockers (nifedipine, diltiazem, Mn ions) and could be reversibly blocked by tetracaine, procaine and benzocaine. Caffeine contractures could also be produced by the ureter muscle placed in isotonic K-solution. Cooling significantly potentiated low-Na, potassium and caffeine contractures of the ureter muscle. Filling of the store is totally dependent on the entry of Ca ions from the extracellular Ca2+ store sites which sequester Ca ions entering the cell on either Na-Ca exchange or via voltage operated Ca channels.
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PMID:Effects of caffeine on the electrical and mechanical activity of guinea-pig ureter smooth muscle. 243 12

Prostaglandins of the E type (PGE) relaxed guinea-pig ureter but prostaglandins of the F type (PGF) did not affect smooth muscle contraction. Hyperpolarization and relaxation of the muscle cells caused by the PGEs were achieved at concentrations in a different range, a feature also observed in the presence of forskolin or iso-butyl-methyl-xanthine (IBMX). Hyperpolarization was inhibited in the presence of k-strophanthoside. The c-AMP content of ureter smooth muscle cells was increased in the presence of PGE2. These observations suggest that the PGE-induced hyperpolarization is caused by activation of the sodium-potassium pump and that enhancement of the cellular c-AMP level plays a major role in the PGE-induced relaxation.
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PMID:The action of prostaglandins on ureter smooth muscle of guinea-pig. 244 83

Lipoxygenase blocker BW755C has been studied for its effect on calcium inward current in intracellularly perfused voltage clamped and contraction of guinea-pig ureter smooth muscle. BW755C increased the Ca inward current in somatic membrane and inhibited contraction of the smooth muscle evoked by high-potassium solution. It is suggested that the effects observed are related to the changes in the level of cyclic nucleotides in cytoplasm due to the action of the final products of lypoxygenase breakdown of fatty acids from the cell membrane.
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PMID:[Effect of the lipoxygenase blockader BW755C on calcium currents in the nerve cell membrane of the snail and on the contractile responses of the ureteral smooth-muscle fibers in the guinea pig]. 245 56

1. The passive and active electrical properties of freshly dispersed single cells of the guinea-pig ureter were investigated using standard patch-clamp techniques. 2. Action potentials, having a rapid rising phase and a prolonged plateau, were recorded on passing depolarizing currents through the patch pipette when 'near-normal' physiological gradients were established across the cell membrane (5.9 mM-K+, 1.5 mM-Ca2+ in the bath; 126 mM-K+ in the pipette). 3. Under voltage clamp, depolarization to potentials positive of -50 mV (from a holding potential of -70 or -80 mV) triggered a net inward current which reached a peak in 5-10 ms and then slowly inactivated. 4. The averaged membrane current to depolarization to potentials between -30 and 0 mV showed two distinct patterns after the peak of the inward current; the membrane current either moved slowly outward over 400 ms or there was one or more transient outward currents superimposed on the slowly decreasing inward current. Both outward currents were blocked when 5 mM-tetraethylammonium (TEA) was added to the bathing solution, resulting in an increased inward current at all potentials. 5. Replacing the extracellular Ca2+ with Co2+ (1.5-5 mM) blocked the inward current and the outward currents to reveal another transient outward current (voltage activated) which activated rapidly to reach a peak within 5 ms and which inactivated exponentially with a time constant of 10 ms. This voltage-activated outward current was inactivated if the membrane was held at -50 mV, but could be reactivated by short hyperpolarizing pre-pulses. The amplitude of this transient current in response to a fixed depolarization (to 0 mV) was half-maximum when the hyperpolarizing pre-pulse was to -66 mV. The voltage-activated outward current was reduced in amplitude when the extracellular potassium was raised to 46 mM or upon exposure to 1 mM-4-aminopyridine (4-AP), but was not affected by 5 mM-TEA. 6. Replacing K+ in the pipette and bathing solution with caesium (Cs) blocked all outward currents, revealing the time course and voltage dependence of the inward current, which could be carried by Ca2+ or Ba2+ with little effect on its rate of inactivation. 7. It was concluded that the inward current recorded in single ureter cells was due to the flow of current through voltage-activated Ca2+ channels. The TEA-sensitive outward currents, whether transient or slowly activating, are presumably K+ channels activated by Ca2+.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Identification of the major membrane currents in freshly dispersed single smooth muscle cells of guinea-pig ureter. 260 Aug 37


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