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)

The arterial vasodilator activity of endothelium-derived relaxing factor (EDRF) is mediated by activation of the soluble form of guanylate cyclase, causing increased levels of guanosine-3',5'-cyclic monophosphate (cGMP). Because of its extreme lability, the actions of EDRF are local. The ability to monitor changes in renal interstitial fluid cGMP would be of great advantage in clarification of local mechanisms controlling renal function. Utilizing a renal interstitial microdialysis technique, we investigated changes in renal interstitial and urinary cGMP in response to right intrarenal arterial administration of the EDRF inhibitor, NG-monomethyl-L-arginine (L-NMMA), in anesthetized dogs (n = 5) in metabolic balance at a sodium intake of 40 mEq/day. Urine was collected directly from the right and left ureter. L-NMMA at 20-60 micrograms/kg/min significantly decreased right renal interstitial and right urinary cGMP levels (p < 0.01) without changing left renal interstitial and urinary cGMP levels (p < 0.01). L-NMMA at 100 micrograms/kg/min decreased both right and left renal interstitial and urinary cGMP levels (p < 0.01). These data demonstrate the ability to monitor renal interstitial cGMP in vivo. There was a dose-dependent decrease in renal interstitial and urinary cGMP in response to intrarenal EDRF inhibition. Additionally, they suggest that EDRF acts as a renal paracrine substance through the modulation of renal interstitial cGMP.
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PMID:Endothelium-derived relaxing factor modulates renal interstitial cyclic GMP. 128 58

Sodium nitroprusside, nitroglycerin and carperitide (alpha-human ANP) all reduced mean blood pressure, but only carperitide increased the hematocrit in rats with bilateral renal artery- and ureter-ligation. NG-Monomethyl-L-arginine, a selective inhibitor of nitric oxide synthesis, elevated the mean blood pressure but did not change the hematocrit significantly. These findings suggest that ANP has a physiological role in regulating circulatory blood volume distinct from that of NO, although both increase intracellular cyclic GMP in the vasculature.
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PMID:Effects of nitric oxide-related compounds and carperitide on hemodynamics and hematocrit in anesthetized rats. 143 45

The metabolic pathway for the synthesis of 2-guanidinoethanol (GEt) was studied in intact mice and isolated perfused rabbit kidneys. GEt excretions in 24-hr urine increased after the intraperitoneal injection of ethanolamine (EA) into mice. Perfusion of isolated rabbit kidneys with EA and L-arginine (Arg) enhanced the GEt excretion from the ureter. This enhancement was observed in an EA concentration-dependent manner under the presence of Arg. When glycine (Gly) was added to the perfusion medium together with EA and Arg, the enhancement of GEt excretion was inhibited, whereas, guanidinoacetic acid excretion was increased to the same extent as during the perfusion with Gly and Arg. These results indicate that GEt is synthesized from Arg and EA in the kidney and that this synthesis is catalyzed by Arg:Gly amidinotransferase (EC 2.1.4.1.). We also described the guanidino compound excretion levels, including levels of GEt, in the rabbit, mouse, rat, and cat. The levels varied considerably with mammalian species.
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PMID:The biosynthesis of 2-guanidinoethanol in intact mice and isolated perfused rabbit kidneys. 379 26

Nitric oxide (NO) has been suggested as a nonadrenergic non-cholinergic neurotransmitter in the urogenital tract and has previously been shown to have a smooth muscle relaxing effect in the urogenital organs both in various animals and in humans. It has been shown that NO is a mediator of the erection and the dilatation of the bladder neck and urethra. The aim of the study was to analyse nitric oxide synthase (NOS) activity in the human urogenital tract. NOS activity was measured by the conversion of L-[U-14C] arginine to L-[U-14C] citrulline. In the upper urinary tract there was Ca(2+)-dependent NOS activity in the renal pelvis, but no significant NOS activity could be found in the ureter. In the lower urinary tract we found high Ca(2+)-dependent NOS activity in the urethra, intermediate activity in the bladder neck and comparatively low activity in the detrusor muscle. In the male genital tract the testis and epididymis had no significant NOS activity. The vas deferens, prostate, seminal vesicle and corpus cavernosum were found to have high levels of Ca(2+)-dependent NOS activity. Ca(2+)-independent NOS activity was not obtained in the urogenital tract. Our results correspond well with previous functional studies indicating NO to be an important nerve-induced mediator of erection and in the micturition reflex, but also suggest that NO may be involved in several other functions in the human urogenital tract.
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PMID:Nitric oxide synthase activity in the human urogenital tract. 753 44

NADPH-diaphorase histochemical staining and electrical field stimulation (EFS) were performed in vitro to investigate whether nitric oxide (NO) is involved in non-adrenergic non-cholinergic (NANC) inhibitory neurotransmission of pig intravesical ureter. NADPH-diaphorase activity was expressed in nerve trunks and thin nerve fibres around arteries and muscular bundles in the intravesical ureter. Relaxations to EFS were tetrodotoxin (10(-6) M)-sensitive which indicates their neurogenic origin. Addition of the NO-synthase inhibitor, L-NG-nitroarginine (L-NOARG, 3 x 10(-5) M), abolished the electrically induced relaxations, which were significantly reversed by L-arginine (3 x 10(-3) M). Addition of acidified sodium nitrite (NaNO2, 10(-5)-10(-3) M) evoked concentration-dependent relaxations of ureteral strips which were unaffected by L-NOARG. It is concluded that NO synthase is present in nerve fibres and NO seems to mediate the inhibitory neurotransmission of the porcine intravesical ureter.
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PMID:Nitric oxide is involved in the non-adrenergic, non-cholinergic inhibitory neurotransmission of the pig intravesical ureter. 778 45

The distribution of acetylcholinesterase (AChE)-positive nerve fibers and cells, as well as the effects of acetylcholine (ACh) on ureteral smooth muscle and small resistance arteries were investigated in the equine ureter by means of histochemical, classic organ baths and myograph techniques. AChE-positive nerve fibers were widely distributed throughout the ureteral wall forming muscular, subepithelial and perivascular nerve plexuses, whose density was highest at the intravesical ureter. AChE-positive nerve cells were also identified grouped as adventitial or intramural ganglia. ACh increased concentration-dependently both the frequency of phasic contractile activity and basal tone of the isolated intravesical ureter, the pD2 values being 6.31 +/- 0.18 and 6.59 +/- 0.13, respectively. The ACh-induced motor effects in ureteral smooth muscle were blocked by atropine, giving pIC50 values of 8.58 +/- 0.08 and 9.68 +/- 0.05 for phasic activity and tone, respectively. Hexamethonium only inhibited ACh-evoked contractile activity at the highest concentration used. ACh elicited a potent endothelium-dependent relaxation of equine ureteral resistance arteries precontracted with 40 mM K-PSS, the pD2 value being 7.94 +/- 0.07. This relaxant response was abolished in the presence of the nitric oxide (NO) inhibitor, NG-nitro-L-arginine (L-NNA), the blockade being reversed by subsequent incubation with the NO exogenous substrate, L-arginine. The ACh-induced relaxation was competitively antagonized by atropine (pA2 = 10.05 +/- 0.18). The present results suggest the existence of a rich cholinergic innervation in the equine ureter which controls both ureteral smooth muscle and resistance arteries motor activity through the muscarinic effects of ACh. In addition, the ACh relaxant response in the ureteral resistance arteries seems to be mediated by NO.
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PMID:Histochemical and functional evidence for a cholinergic innervation of the equine ureter. 791 46

1. To define further the role of nitric oxide (NO) in urinary tract function, we have measured the presence of nitric oxide synthase (NOS) activity, and its relationship with functional NO-mediated responses to electrical field stimulation (EFS) in the urethra, the detrusor and the ureter from sheep. NOS activity was assayed by the conversion of L-[14C]-arginine to L-[14C]-citrulline. Endogenous production of citrulline was confirmed by thin layer chromatography. 2. NOS enzymatic activity was detected in the cytosolic fraction from tissue homogenates with the following regional distribution (pmol citrulline mg-1 protein min-1): urethra (33 +/- 3.3), detrusor (13.1 +/- 1.1) and ureter (1.5 +/- 0.2). No activity was detected in the particulate fraction of any region. 3. NOS activity was dependent on Ca(2+)-calmodulin and required exogenously added NADPH and tetrahydrobyoptein (BH4) for maximal activity. Exclusion of calmodulin from the incubation mixture did not modify NOS activity, but it was significantly reduced in the presence of the calmodulin antagonist, calmidazolium, suggesting the presence of enough endogenous calmodulin to sustain the observed NOS activity. 4. NOS activity was inhibited to a greater extent by NG-nitro-L-arginine (L-NOARG) and its methyl ester (L-NAME) than by NG-monomethyl-L-arginine (L-NMMA), while 7-nitroindazole (7-NI) was a weak inhibitor and L-cannavine had no effect. 5. Citrulline formation could be inhibited by superoxide dismutase in an oxyhaemoglobin-sensitive manner, suggesting feedback inhibition of NOS by NO. 6. EFS induced prominent NO-mediated relaxations in the urethra while minor or no responses were observed in the detrusor and the ureter, respectively. Urethral relaxations to EFS were inhibited by NOS inhibitors with the rank order of potency: L-NOARG = L-NAME > 7-NI > L-NMMA. 7. In conclusion, we have demonstrated the presence of NO-synthesizing enzymatic activity in the sheep urinary tract which shows similar characteristics to the constitutive NOS isoform found in brain. We suggest that the enzymatic activity measured in the urethral muscle layer may account for the NO-mediated urethral relaxation during micturition whereas regulation of detrusor and ureteral motor function by NOS containing nerves is less likely.
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PMID:Characterization of nitric oxide synthase activity in sheep urinary tract: functional implications. 879 61

Angiotensin-converting enzyme (ACE) inhibitors have been shown to minimize fibrosis of the kidney tubulointerstitium in several diseases. In addition to lowering angiotensin II levels, ACE inhibitors can increase kinin levels and subsequently increase nitric oxide formation. To determine whether nitric oxide generation is a component of the beneficial effect of ACE inhibitors on renal fibrosis, enalapril, enalapril plus NG-nitro-L-arginine methyl ester (L-NAME) or L-arginine was administered to rats that had undergone unilateral ureteral obstruction (UUO). Ureteral obstruction caused significant increases in interstitial volume, monocyte macrophage infiltration, interstitial collagen IV and alpha-smooth muscle actin expression, transforming growth factor-beta 1 mRNA, collagen IV mRNA, and tissue inhibitor of metalloproteinase-1 mRNA. Enalapril treatment significantly blunted the increase in all parameters during UUO. Cotreatment of the animals with enalapril and L-NAME reversed the beneficial effect of enalapril in the obstructed kidney for all parameters. Treatment of animals with UUO with L-arginine significantly blunted the increase in all parameters except for transforming growth factor-beta 1 mRNA expression. In the enalapril- plus-L-NAME-treated animals, there were modest but significant increases in monocyte/macrophage infiltration of the interstitium and glomerulus, and collagen IV and alpha-smooth muscle actin expression in the interstitium of the contralateral unobstructed kidney. The urine nitrite concentration was significantly increased by either enalapril or L-arginine treatment, whereas L-NAME significantly reduced urine nitrite concentration. These results suggest that treatment modalities that increase nitric oxide formation have a beneficial effect on the progression of cellular and molecular parameters of tubulointerstitial fibrosis caused by obstruction of the ureter.
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PMID:Nitric oxide generation ameliorates the tubulointerstitial fibrosis of obstructive nephropathy. 891 81

The distribution of nitric oxide synthase (NOS)-immunoreactive (IR) and haemoxygenase (HO)-IR nerves was investigated in the pig and human intravesical ureter (IVU). NOS activity was measured by monitoring the conversion of [3H]-arginine to [3H]-citrulline. Effects of NO and resulting changes in cyclic nucleotide concentrations were assessed in vitro. The effects of carbon monoxide (CO) on IVU motility was also tested. Immunohistochemistry revealed an abundant overall innervation of the IVU and numerous NOS-IR nerves. Nerve trunks were also found expressing immunoreactivity for HO-1, one of the enzymes synthetising CO. Similar profiles of nerve structures expressing immunoreactivities for NOS and tyrosine-hydroxylase (TH), as well as NOS and vasoactive intestinal peptide (VIP) were demonstrated. In the pig IVU, measurement of NOS activity revealed a moderate calcium-dependent catalytic activity, NO and the NO-donor SIN-1 reduced in a concentration-dependent manner serotonin-induced contractions of pig and human IVU, and the spontaneous contractions of pig IVU. In pig IVU strips precontracted with the thromboxane analogue U-46619, tetrodotoxin-sensitive relaxations were abolished by the NOS inhibitor NG-nitro-L-arginine. CO exerted no significant effect on spontaneous or induced contractions in the pig and human IVU. In precontracted strips of the pig and human IVU exposed to SIN-1 or NO, significant increases of cyclic GMP levels were measured in comparison to control preparations. The results suggest that the L-arginine/NO/cyclic GMP pathway may play a role in the regulation of the valve function in the uretero-vesical junction (UVJ). A role for CO in the UVJ has yet to be established.
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PMID:Localization of nitric oxide synthase and haemoxygenase, and functional effects of nitric oxide and carbon monoxide in the pig and human intravesical ureter. 913 43

1. The effects of circumferentially-applied stretch on the spontaneous contractility of a whole mount preparation of the guinea-pig upper urinary tract (UUT) (renal pelvis and ureter) were investigated by use of standard isometric tension recording techniques. 2. Simultaneous tension recordings of the proximal and distal portions of the renal pelvis (RP) and ureter revealed that spontaneous contractions, in 79% (n = 66) of preparations, originated in the proximal RP (at a frequency of 4.5 min(-1)) and propagated to the distal RP and ureter at a velocity of 1-3 cm s(-1). Pretreatment with tetrodotoxin (TTX) (3-10 microM) or N(G)-nitro-L-arginine (100 microM) had little effect on the spontaneous contractility of the UUT, motility indexes (MIs) (contraction amplitude x contraction frequency) calculated after 20 min exposure were little affected by TTX or N(G)-nitro-L-arginine (L-NOARG). Omega-conotoxin GVIA (100 nM) significantly reduced MI values in both the proximal RP and ureter. 3. Exposure of the spontaneously-active UUT to capsaicin (10 microM for 15 min) induced a transient increase in UUT contractility, followed by a prolonged negative inotropic effect. The MI values, calculated 60 min after the washout of capsaicin, for the proximal and distal RP and ureter were reduced to 56%, 53% (n = 18) and 61% (n = 16), respectively, of their control values. This capsaicin pretreatment blocked the positive inotropic effects of transmural electrical nerve stimulation on UUT contractility to reveal a small inhibitory effect which was readily blocked by tetrodotoxin (3 microM) (n = 3). The excitatory and inhibitory actions of nerve stimulation were both blocked by TTX (3 microM). 4. A second exposure to capsaicin (10 microM for 15 min), further reduced the MI values (calculated 60 min after washout) in the proximal and distal RP to 41% and 31%, respectively (n = 6; P<0.05), of the initial control values. 5. In 61% (n = 99) of preparations, the application of stretch to the proximal RP (0.5 to 2 mm) evoked a decrease in the amplitude of the contractions recorded in the distal RP, but not in the ureter. Stretch applied to the distal RP or ureter had no effect on the contractions recorded in the other regions of the UUT. 6. In 5 out of 6 preparations, a single application of capsaicin (10 microM for 15 min) had little effect on the change in contractile force of the distal RP evoked upon stretch of the proximal RP. 7. The inhibition of the distal RP upon stretch of the proximal RP was partially reduced (P<0.05) when the UUT was pretreated with the calcitonin gene-related peptide (CGRP) receptor antagonist, hCGRP (8-37) (1 microM). 8. The application of the CGRP receptor agonist, hCGRP (100 nM) inhibited contractility in the UUT in a region dependent manner. The MI of the proximal RP was decreased 32% after 6 min; while the MIs of the distal RP and ureter were reduced 83% and 63%, respectively, within 5 min of the application of hCGRP. 9. Glibenclamide (1 microM) had little effect on the spontaneous contractility of the UUT, but significantly reduced the inhibition of the distal RP evoked upon stretch (0.5 to 2 mm) of the proximal RP. TTX (3-10 microM), L-NOARG (100 microM) or omega-conotoxin GVIA (100 nM) had little effect on the stretch-evoked inhibition of the distal RP. 10. It was concluded that circumferential stretch of the proximal RP inhibits the contractility of the distal RP and that a component of this inhibition involves the activation of a glibenclamide-sensitive mechanism via the release of endogenous CGRP, possibly from the varicosities of intramural sensory nerves.
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PMID:Stretch-evoked inhibition of spontaneous migrating contractions in a whole mount preparation of the guinea-pig upper urinary tract. 955 98

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