UMLS:C0403608 - FACTA Search

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

Adenylate cyclase and phosphodiesterase enzyme activities were demonstrated in rabbit ureter. NaF, 10 mM, caused a 60.9 per cent increase in adenylate cyclase activity. Isoproterenol, 5 X 10-7 to 10-5 M induced a statistically significant dose-dependent increase in adenylate cyclase activity which was suppressed by propranolol, 10-7 M. Theophylline, 5 X 10-5 to 10-2 M, significantly inhibited phosphodiesterase activity. Thus, isoproterenol and theophylline, two agents that can relax ureteral segments previously contracted by a depolarizing concentration of potassium, could presumably increase cyclic AMP levels, isoproterenol by increasing synthesis and theophylline by decreasing degradation.
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PMID:Adenylate cyclase and phosphodiesterase activity in rabbit ureter. 19 62

The hyperchloremic metabolic acidosis which can occur following urinary diversion through intestinal segments has been managed with bicarbonate or citrate salts. However, satisfactory management is not always possible with this form of treatment. The development of this acidosis has been attributed to intestinal reabsorption of urinary solutes or intestinal secretion of bicarbonate. Intestinal absorptive and secretory processes are modulated by an adenylate cyclase-cyclic AMP system. Chlorpromazine inhibits the effect of cyclic AMP on the intestinal mucosal cell. The use of chlorpromazine in the management of the hyperchloremic metabolic acidosis following urinary diversion was investigated. A canine model employing an ileal segment between ureter and bladder and a rat model in which urine is diverted through the entire colon have been developed. Chlorpromazine (5 mg./kg./day) was found to be efficacious in the management of the metabolic derangements that occur in both of these models. A case study is presented in which conventional management of this syndrome with bicarbonate salts was unsuccessful. The use of chlorpromazine as an adjuvant treatment allowed correction of the acidosis.
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PMID:Chlorpromazine: adjuvant therapy for the metabolic derangements created by urinary diversion through intestinal segments. 298 65

The adenylate cyclase activity in the rabbit renal pelvis and ureter was measured by the method of Salomon et al. (1974). The dobutamine-induced increase of adenylate cyclase activity is more prominent in the renal pelvis including the pacemaker region than in the ureter that is non-pacemaker region in the upper urinary tract. Therefore, it is thought that the pacemaker region is different from other regions in the upper urinary tract with regard to responses to dobutamine.
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PMID:Effect of dobutamine on adenylate cyclase activity in rabbit renal pelvis and ureter. 370 60

Research on the physiopathologic and biochemical nature of prostaglandins (PGs) suggest that PGs play a role in reproductive physiology. In vitro studies show that the PGE series decrease the motility of the human uterus, fallopian tubes, and ureter, and produce vasodilatation. PGFs cause vasoconstriction and increased motility of the uterus, fallopian tubes, ureter, and gastrointestinal muscle. PGs are also known to inhibit lipolysis, platelet aggregation, and gastric secretion. The exact mechanism of PGs are not fully understood, but evidence suggests that many responses can be attributed to interference with the enzyme adenyl cyclase, which catalyzes the formation of adenosine 3',5'-monophosphate (cyclic AMP) from adenosine triphosphate. The adenyl cyclase-cyclic AMP system mediates lipolysis, steroidogenesis, gastric secretion, certain smooth muscle motility responses, and increase in permeability due to vasopressin. Early studies of the myometrial effects of PGs showed that the PGE series inhibited the motility of the human myometrium in vitro while the PGF series produced mixed responses. The role of PGF2alpha in parturition has not been established but evidence suggests that it has a potential role as an oxytocic in cases of therapeutic abortion. In the area of human fertility, the physiologic role of PGs in seminal fluid is hypothesized to facilitate the migration of spermatozoa from the vagina into the uterine cavity. Karolinska Institute researchers have found that some infertile males have low PG levels in their ejaculates and are now working with methods of improving the PG levels to improve their fertility. Pickles et al. proposed a potential role for PGs in the etiology of dysmenorrhea, having found a significantly higher ratio of PGF to PGE in a series of patients with severe dysmenorrhea than in a comparable series of normal patients. The luteolytic and antinidatory effects of PGF2alpha are being investigated and studies appear encouraging. PGs have therapeutic potentials in induction of labor, treatment of infertility, morning-after conception, treatment of dysmenorrhea, and contraception by alteration of fallopian tube motility.
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PMID:The role of prostaglandins in reproductive physiology. 491 53

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

Effects of prostaglandin E1, E2 and F2 alpha (PGE1, PGE2 and PGF2 alpha) on the changes in the adenylate cyclase (AC) activities of rabbit urinary tract tissues were studied in order to clarify whether the PGs' actions are mediated by cAMP in the urinary tract. AC activities were measured by the method of Salomon et al. The three PGs studied were all found to increase the AC activities dose-dependently in the renal pelvis, ureter, bladder dome and bladder base. Among the changes in AC activities, PGE1 and PGE2 significantly increased the AC activities of the renal pelvis and ureter. PGE1 significantly increased the AC activities of the bladder dome. It was reported that Ca2+ influx plays an important role in the PGs' action on the urinary tract. Our data suggest that the PGs act on the urinary tract via cAMP as well as Ca2+ influx.
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PMID:[Effects of prostaglandin E1, E2 and F2 alpha on the changes in the adenylate cyclase activities of rabbit urinary tract tissues]. 838 21

The first measurements of AVT-sensitive adenylate cyclase activity in specific segments of the nephron of the Australian arid-zone agamid lizard, Ctenophorus (=Amphibolurus) ornatus, are reported. All sections of the collecting-duct system of this lizard were found to be sensitive to AVT at a concentration of 1 x 10(-6) M. In addition, receptors to AVT were located in the thin-intermediate segment linking proximal and distal convoluted tubules. No significant response to AVT was detected in the glomeruli, in either proximal or distal convoluted tubules, or in the ureter. The physiological significance of these particular segments is discussed in terms of the action of AVT in stimulating water and salt reabsorption in the lizard kidney.
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PMID:Arginine vasotocin: locus of action along the nephron of the ornate dragon lizard, Ctenophorus ornatus. 881 98

Pituitary adenylate cyclase activating peptide is a new member of the vasoactive intestinal polypeptide family of peptides which is present in the brain as well as neuronal elements of a number of peripheral organs. Pituitary adenylate cyclase activating peptide occurs in two forms, pituitary adenylate cyclase activating peptide-38 and the C-terminally truncated 27 amino acid form, pituitary adenylate cyclase activating peptide-27, both derived from the same precursor which in addition gives rise to a structurally-related peptide, pituitary adenylate cyclase activating peptide-related peptide. Using specific radioimmunoassays for pituitary adenylate cyclase activating peptide-38, pituitary adenylate cyclase activating peptide-27 and pituitary adenylate cyclase activating peptide-related peptide we found that all three pituitary adenylate cyclase activating peptide-precursor-derived peptides were present in tissue extracts from the ureter, the urinary bladder and the urethra. Pituitary adenylate cyclase activating peptide-38 was the dominating peptide with the highest concentration in the ureter. When extracts from the urinary bladder were fractionated by reverse phase high pressure liquid chromatography immunoreactive components corresponding to synthetic pituitary adenylate cyclase activating peptide-38, pituitary adenylate cyclase activating peptide-27 and pituitary adenylate cyclase activating peptide-related peptide were identified with the respective antisera. By immunohistochemistry, using a specific monoclonal mouse anti-pituitary adenylate cyclase activating peptide antibody, pituitary adenylate cyclase activating peptide-immunoreactivity was shown to have a widespread distribution in the rat urinary tract, localized exclusively to nerve fibres. No immunoreactive neuronal cell bodies were observed in any of the tissues. Pituitary adenylate cyclase activating peptide was shown to be located in varicose nerve fibres associated with blood vessels and smooth muscle. The majority of pituitary adenylate cyclase activating peptide-positive nerve fibres and bundles were, however, present in subepithelial plexuses from which delicate varicose nerve fibres entered the urothelium. Double immunostaining for pituitary adenylate cyclase activating peptide and a marker for sensory neurons, calcitonin-gene related peptide, disclosed that the two peptides were almost completely co-localized while the co-existence between pituitary adenylate cyclase activating peptide and the structurally related peptide vasoactive intestinal polypeptide, was scarce. Neonatal capsaicin-treatment caused a marked reduction in the concentration of immunoreactive pituitary adenylate cyclase activating peptide in all regions of the rat urinary tract, being most prominent in the ureter. By immunohistochemistry it was shown that the sensory neurotoxin caused a reduction in the number and intensity of pituitary adenylate cyclase activating peptide-immunoreactive nerve fibres in all organs of the urinary tract which was most prominent in the epithelial and subepithelial layers. Identical changes were observed for the calcitonin-gene related peptide-containing nerve fibres, while vasoactive intestinal polypeptide-positive nerve fibres were unaffected by capsaicin-treatment. In conclusion pituitary adenylate cyclase activating peptide is present in the rat urinary tract mainly in the form of pituitary adenylate cyclase activating peptide-38. Immunoreactive nerve fibres were associated with the epithelium, blood vessels and smooth musculature. Pituitary adenylate cyclase activating peptide was almost completely co-localized with calcitonin-gene related peptide and by neonatal capsaicin treatment the two peptides were identically affected. The findings suggest that pituitary adenylate cyclase activating peptide is a sensory neurotransmitter in the rat urinary tract.
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PMID:Pituitary adenylate cyclase activating polypeptide immunoreactivity in capsaicin-sensitive nerve fibres supplying the rat urinary tract. 950 64

The presence, distribution and colocalisation of pituitary adenylate cyclase activating peptide (PACAP) immunoreactivity have been studied in the duck ureter by using Western blot analysis, radioimmunoassays (RIA) and immunohistochemistry. The presence of both PACAP-38 and PACAP-27 was demonstrated, PACAP-38 being the predominant form. PACAP-immunoreactive fibres and neurons were found in all the ureteral layers. Double immunostaining showed that PACAP was almost completely colocalised with vasoactive intestinal peptide (VIP). Moreover, PACAP was found in substance P (SP)-containing ureteral nerve fibres and in SP-containing dorsal root ganglion neurons. RIA performed on denervated ureters demonstrated that almost half of the ureteral PACAP was extrinsic in origin. These findings suggest that, in birds, PACAP has a role in diverse nerve-mediated ureteral functions.
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PMID:Pituitary adenylate cyclase activating peptide (PACAP) immunoreactivity in the ureter of the duck. 1157 87

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