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

I have investigated the effects of autonomic drugs and prostaglandins on in vitro smooth muscle spontaneous contractions and made the quantitative analysis of autonomic receptors in the canine ureter. Ureteral muscle strip cut helically usually generated spontaneous contractions whereas those cut circularly or longitudinally did not generate spontaneous contractions. These results suggest the importance of knowing which direction to cut the ureteral smooth muscle in order to generate spontaneous contractions. Norepinephrine (alpha), phenylephrine (alpha 1), carbachol (muscarinic) and PGF2 alpha caused significant increase in contractile force. Terbutaline (beta 2) and PGE2 caused significant decreases in contractile force, while dobutamine (beta 1) and clonidine (alpha) caused no effect. Autonomic receptor densities were determined using radiology and binding techniques. The number of maximum binding sites (Bmax) of 3H-prazosin (PZ), 3H-yohimbine (YOH), 3H-dihydroaloprenolol (DHA) and 3H-quinuclidinylbenzilate (QNB) were 53.8, 16.9, 11.2 and 5.28 fmol/ml protein, respectively. These data suggest that the contractile responses to adrenergic and cholinergic agonists in the canine ureter are mediated through functional adrenergic (alpha 1, beta 2) and muscarinic cholinergic receptors and that the prostaglandins have a role in the contraction of the canine ureter.
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PMID:[The function of autonomic receptors in canine ureteral smooth muscle]. 166 83

An intact canine model was developed to study the effects of prostaglandins (PG) and prostaglandin synthetase inhibitors on acutely obstructed kidneys. Totally implanted nephrostomy tubes were placed to measure renal pelvic pressure. Complete ureteral obstruction was obtained with a Fogarty balloon catheter inflated in the distal ureter; by this method renal pelvic pressure reached 40-50 mm Hg. Renal pelvic pressure was reduced after intravenous indomethacin and dipyrone administration, whereas blood pressure showed no major changes. Exogenous prostaglandins had both immediate and contrary effects: PGE2 caused a significant decrease, whereas PGF2 alpha caused a significant increase in renal pelvic and blood pressure. The reduced rise in renal pelvic pressure appears to be the main reason for the analgesic effects of prostaglandin synthetase inhibitors. The efficiency of these drugs in the treatment of renal colic is supported by this study, that of prostaglandins cannot be proved.
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PMID:Effects of prostaglandins and prostaglandin synthetase inhibitors on acutely obstructed kidneys in the dog. 179 8

Prostaglandin synthetase inhibitors are used for the treatment of ureteric colic. However, there is controversy regarding the mechanism of action of these drugs. In this study, differential prostaglandin synthesis in the human renal pelvis, ureter and bladder was measured using specific radioimmunoassays and gas chromatography/mass spectrometry. There was a significant quantitative predominance of the smooth muscle constrictor eicosanoids, PGF2 alpha and TXA2 over the dilatory PGE2 in tissue from all sites--renal pelvis, ureter and bladder. The results indicate that prostaglandins play a direct role in smooth muscle activity of the upper urinary tract and the inhibition of this activity with indomethacin indicates a further mode of its action in pain relief in ureteric colic.
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PMID:Eicosanoid synthesis in the isolated human renal pelvis, ureter and bladder. 202 8

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

Prostaglandin E2 (PGE2) and 16,16-dimethyl PGE2 (16,16-dm PGE2) caused contraction of guinea-pig taenia caeci, contraction and at higher concentrations relaxation of trachea and relaxation of ureter smooth muscle. The prostacyclin derivative iloprost induced contraction of taenia caecum, while it was inactive in the other preparations. After pretreatment of the smooth muscles with 16,16-dm PGE2, stimulation of the PGE2 receptors in taenia caeci and trachea and of PGI2 receptors in taenia caeci caused relaxation. The results indicate that the prostanoid receptor mediating contraction is selectively vulnerable for desensitization in contrast with the receptor mediating smooth muscle relaxation.
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PMID:Desensitization of PGE2 and PGI2 induced contractions in different smooth muscles of guinea-pig unmasking relaxing properties of prostanoids. 245 36

The renal excretion of prostaglandins E2 and 6-keto-F1 alpha, thromboxane B2 and cyclic adenosine 3', 5'-monophosphate was measured in a solitary kidney model of chronic ureteral obstruction in rabbits. The presence of obstruction was confirmed by intravenous pyelography. Growth rate of the animals and furosemide-stimulated diethylenetriaminepentaacetic acid renography were used to grade the obstruction. As correlated to urinary creatinine concentration the excretion of 6-keto-PGF1 alpha dominated in nephrectomized, unobstructed control animals. With the degree of ureteral obstruction becoming more severe, the output of PGE2 increased, while that of 6-keto-PGF1 alpha and TxB2 decreased. As a result the ratios PGE2/6-keto-PGF1 alpha and PGE2/TxB2 were three times as high in severely obstructed rabbits as in control animals. The renal output of cyclic AMP was unaffected by chronic obstruction. We conclude that the renal metabolism of prostanoids is affected in a unique way in chronic partial obstruction of the ureter.
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PMID:Renal excretion of prostanoids and cyclic AMP in chronic partial ureteral obstruction of the rabbit. 253 44

The mechanism of the increased prostaglandin production and induction of sensitivity to bradykinin by the cortex of the hydronephrotic rabbit kidney was investigated using tissue culture techniques. Cortical interstitial cells from normal, unilaterally hydronephrotic and contralateral kidneys were grown in tissue culture. Cells derived from hydronephrotic kidneys, but not normal or contralateral, increased PGE2 production when incubated with bradykinin. Of the two cell types, fibroblasts and macrophages, grown from hydronephrotic explants, neither increased prostaglandin production when grown alone in tissue culture. Recombining the two cell types restored bradykinin responsiveness. Bradykinin responsiveness could be induced in either normal or contralateral cell cultures when macrophages from the hydronephrotic kidney were added to cultures of cells from normal or contralateral cortex. The data indicate unique characteristics of hydronephrotic macrophages are involved in the induction of bradykinin responsiveness in the cortex of the ureter-ligated kidney.
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PMID:Cortical interstitial cell interactions induce sensitivity of hydronephrotic kidney to bradykinin. 316 39

The effect of micropuncture of the renal papilla through an intact ureter on urinary concentrating ability of rats was examined. Micropuncture of the renal papilla caused a fall in urine osmolality in the punctured kidney from 1718 +/- 106 to 1035 +/- 79 mosmol/kg X H2O. In order to investigate the role of renal prostaglandins in this process, PGE2 excretion was measured and found to increase from 63.4 +/- 14.0 to 205.5 +/- 57.1 pg/min. Urine osmolality and PGE2 excretion from the contralateral kidney were not significantly altered. In animals given meclofenamate (2 mg/kg X hr), renal PGE2 excretion was reduced to 22.3 +/- 5.1 pg/min prior to micropuncture and it remained low at 8.9 +/- 1.8 pg/min after papillary micropuncture. Meclofenamate also blocked the fall in urine osmolality caused by micropuncture of the renal papilla, with urine osmolality averaging 1940 +/- 122 before and 1782 +/- 96 mosmol/kg X H2O after the micropuncture. These results indicated that papillary micropuncture through an intact ureter increased renal PGE2 excretion and that a rise in renal production of PGE2 or some other prostanoid is associated with a fall in urine concentrating ability.
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PMID:Role of renal prostaglandins in the fall in urine osmolality after papillary micropuncture. 386 79

In the present study, metabolism of prostaglandins (PGs) by 15-hydroxyprostaglandin dehydrogenase (15-OH PGDH) was investigated in dog kidneys with ureteral obstruction. After 24 hr of ureteral obstruction, the obstructed kidney and the contralateral kidney were removed and the cytosolic fractions (105,000 X g), enriched in 15-OH PGDH, were prepared from the cortex and medulla. 15-OH PGDH activity was estimated by radiometric assays of the metabolism of [3H]PGE2 and [3H]prostacyclin. Cortical 15-OH PGDH activity decreased by greater than 50% in the ureter-obstructed kidney as compared to the contralateral kidney. Similar results were obtained by estimating the stereo-specific release of tritium from position 15 using 15-[3H]PGF2 alpha as substrate. In contrast to the cortex, there were no differences in 15-OH PGDH activity found in the medulla of the obstructed and contralateral kidneys. Because the cortex contains higher levels of 15-OH PGDH activity, the deficiency in that site may contribute to the elevated levels of PGs in renal venous blood during ureteral obstruction.
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PMID:Deficiency in 15-hydroxyprostaglandin dehydrogenase activity after unilateral ureteral obstruction of the dog kidney. 388 82

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


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