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

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 distribution and patterns of colocalization of nitric oxide synthase (NOS), vasoactive intestinal peptide (VIP), neuropeptide Y (NPY) and the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH) were examined in nerve fibers supplying the human lower ureter using double label immunofluorescence. Many nerve fibers immunoreactive for NOS were observed within the ureter. Positive varicose fibers were seen running longitudinally within the smooth muscle bundles, particularly those of the inner layers of the ureter. Immunoreactive axons were also prominent within the subepithelium, and as plexi surrounding many blood vessels. The colocalization studies indicated that NOS was never present in presumptive sympathetic nerve fibers expressing TH. All fibers containing VIP, however, were also immunoreactive for NOS. In addition, a minor population of NOS fibers did not contain VIP. Neuropeptide Y coexisted with NOS in a significant number of nerve terminals, although fibers expressing only NPY were equally common. Several immunochemically distinct nerve populations can therefore be distinguished in the human ureter: (1) nerves containing NOS either with or without VIP; (2) NOS-immunoreactive fibers with NPY; and (3) those fibers expressing TH or NPY which do not contain NOS. The results indicate that some non-noradrenergic peptide-containing nerves in the human ureter have the capacity to synthesize nitric oxide (NO), and that NO may be involved in the regulation of ureteric motility.
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PMID:Colocalization of nitric oxide synthase with vasoactive intestinal peptide, neuropeptide Y, and tyrosine hydroxylase in nerves supplying the human ureter. 752 Sep 52

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

1. We have assessed the effect of L-nitroarginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, on hypotension and plasma protein extravasation produced by i.v. administration of substance P (SP) in urethane-anaesthetized rats. 2. I.v. administered SP (1 nmol kg-1) produced maximal blood pressure lowering effect which was not modified by previous administration of L-NOARG (45.6 mumol kg-1 i.v.). The hypotensive response to SP was greatly reduced by the nonpeptide SP antagonist, RP 67,580 (0.68 mumol kg-1) indicating the involvement of tachykinin NK-1 receptor. L-NOARG caused by itself a sustained increase in both systolic and diastolic blood pressure, while RP 67,580 was without effect. 3. I.v. administration of SP produced plasma protein extravasation in the trachea, ureter and urinary bladder (determined by the Evans blue leakage technique). A dose of 10 nmol kg-1 SP was necessary to produce a maximal effect, while the tachykinin NK-1 receptor selective agonist [Sar9]SP sulphone produced a similar maximal response at 3 nmol kg-1 in the various organs tested. 4. L-NOARG failed to affect plasma protein extravasation produced by either SP or [Sar9]SP sulphone while RP 67,580 inhibited the response to both agents. 5. The present findings fail to reveal a significant contribution of NO production in the hypotensive and inflammatory response to NK-1 receptor stimulation in urethane-anaesthetized rats.
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PMID:Failure of L-nitroarginine, a nitric oxide synthase inhibitor, to affect hypotension and plasma protein extravasation produced by tachykinin NK-1 receptor activation in rats. 768 68

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

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

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

The aim of the study was to ascertain whether nitric oxide (NO) might regulate motility in the human upper urinary tract. Smooth muscle activity in the human renal pelvis and proximal ureter was studied in vitro in organ baths, and nitric oxide synthase (NOS) activity was studied by measurement of citrulline formation. NO, glyceryl trinitrate (GTN) and sodium nitroprusside (SNP) significantly reduced the frequency of spontaneous rhythmic contractions in renal pelvis and proximal ureter. Exogenously applied NO elicited relaxations in pre-contracted renal pelvis. Calcium-dependent NOS activity was significant in the renal pelvis but undetectable in the ureter. Also, NOS activity was absent in hydronephrotic renal pelvis. NO, SNP and GTN inhibited smooth muscle activity in the human upper urinary tract. NOS activity was obtained in normal renal pelvis but not in hydronephrotic renal pelvis. Regulation of urinary tract NO concentrations might offer a strategy for treatment of renal colic and disturbances in upper urinary tract motility.
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PMID:Modulation of smooth muscle activity by nitric oxide in the human upper urinary tract. 878 78

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

Neurones in the ureterovesical ganglion complex provide autonomic innervation to the pelvic ureter, the ureterovesical junction and the bladder trigone. We examined the distribution and peptide co-expression pattern of nitric oxide synthase (NOS) in the human ureterovesical ganglia by combining NADPH-diaphorase histochemistry with immunoreactivity for vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), and calcitonin gene-related peptide (CGRP). Less than 20% of nerve cells in the large ganglia of the ureterovesical complex were stained for NOS activity. In elderly individuals, ganglion cells regularly exhibited conspicuous morphological alterations suggestive of degenerative changes. Most of the NOS-positive cell bodies costained for VIP-immunoreactivity. A minority of NOS-expressing cells also reacted for NPY-immunoreactivity. CGRP-immunoreactivity was present in varicose terminal-like nerve fibres which were found to encircle NOS-containing perikarya. Occasionally, NOS-positive somata were surrounded by plexiform axon terminals which immunostained for VIP or NPY. We conclude that the passage of urine across the ureterovesical junction is under relaxatory control of a local nitric oxide/VIP(NPY) pathway which may be modulated by preganglionic efferent and/or primary afferent input.
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PMID:Colocalisation of NADPH-diaphorase with neuropeptides in the ureterovesical ganglia of humans. 886 54


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