Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of capsaicin, substance P (SP) and neurokinin A (NKA) on motor activity and vascular permeability was investigated in the rat lower urinary tract (bladder dome and neck, proximal urethra and ureters). Capsaicin produced contractions of the rat bladder dome and neck and of the proximal urethra in vitro, which were unaffected by tetrodotoxin and abolished by ganglionectomy. SP and NKA were almost equipotent in producing a contraction of the rat isolated bladder dome or neck and urethra. However, the maximal response to NKA was about twice that of SP on the urethra and bladder neck. Capsaicin did not affect motility of the unstimulated rat isolated ureter, while NKA or SP activated rhythmic contractions, NKA being about 850 times more potent than SP. Either capsaicin or field stimulation produced a transient inhibition of the NKA-activated rhythmic contractions of the rat isolated ureter which was prevented by capsaicin-desensitization. The capsaicin-(1 microM) or field stimulation-induced inhibition of NKA-activated rhythmic contractions of the rat isolated ureter were unaffected by removal of pelvic ganglia but abolished by cold storage (72 h at 4 degrees C). Intravenous capsaicin induced an inflammatory response (Evans blue leakage) in the bladder, proximal urethra and ureters in vivo. Plasma extravasation was greater in the ureters, urethra and bladder neck than in the dome. SP, NKA and histamine produced a dose-dependent dye leakage in all segments of the rat urinary tract, the response being slightly greater in the bladder neck than in the dome. The capsaicin-induced inflammatory response was abolished by systemic capsaicin-desensitization and reduced, to a variable extent, by pelvic ganglionectomy, in the various tissues examined. Topical application of tetrodotoxin on the bladder dome failed to affect the capsaicin-induced plasma extravasation in the urinary bladder. These findings indicate that chemoceptive, capsaicin-sensitive nerves are present throughout the whole rat lower urinary tract and their activation determines a variety of visceromotor responses and an increase of vascular permeability. In various instances the response to capsaicin may be explained by the action of tachykinins but some effects may involve other sensory neuropeptides.
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PMID:Regional differences in the effects of capsaicin and tachykinins on motor activity and vascular permeability of the rat lower urinary tract. 244 29

Either intra-arterial or topical administration of calcitonin gene-related peptide (CGRP) had little effect on motility of the urinary bladder in urethane-anaesthetized rats. Only a high concentration (50 microM) of topical CGRP activated the micturition reflex and potentiated the response to exogenous substance P (SP). In the isolated rat bladder CGRP had inconsistent effects on spontaneous or field-stimulated contractions. CGRP neither produced any significant plasma extravasation (Evans blue leakage) in the rat lower urinary tract, nor potentiated the response to exogenous SP. CGRP inhibited motility in the rat isolated proximal urethra and ureters and counteracted the contractile response to neurokinins. An inhibitory effect of capsaicin on stimulated motility of the urethra was observed in all preparations and a small contractile response was evident in about 40% of cases. Lack of desensitization to the action of CGRP prevented the study of its interaction with capsaicin. The inhibitory effect of CGRP in the ureter exhibited a specific desensitization: if the preparations were pre-exposed to exogenous CGRP, the inhibition of motility produced by antidromic activation of the capsaicin-sensitive nerve terminals (field stimulation) as well as the response to capsaicin (1 microM) was prevented but the inhibitory response to isoprenaline was unaffected. These findings indicate that CGRP is able to influence markedly the motility of the rat lower urinary tract, but exhibits marked regional differences in its action. Endogenous CGRP could be the inhibitory transmitter which, when released from capsaicin-sensitive fibers, participate in the control of ureteral motility.
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PMID:Visceromotor responses to calcitonin gene-related peptide (CGRP) in the rat lower urinary tract: evidence for a transmitter role in the capsaicin-sensitive nerves of the ureter. 282 87

Intravenous injection of compound 48/80 (1 mg X kg-1) induced an acute increase in vascular permeability to plasma proteins in various organs of rats. The compound 48/80 response was partly inhibited by histamine H1 and H2 receptor blockade in the urinary bladder and in the duodenum, but not in the trachea, the oesophagus, the ureter and the paw skin. Blockade of 5-hydroxytryptamine receptors with methysergide led to a reduction of the permeability response in the oesophagus and in the urinary bladder, leaving responses in other organs unchanged. Pretreatment of neonatal rats with capsaicin almost abolished the 48/80 response in all organs except in the duodenum. Pretreatment of rats with [D-Arg1, D-Trp7,9, Leu11]-substance P, a substance P antagonist, also caused a partial inhibition of the permeability response to compound 48/80 in several organs. Topical administration of compound 48/80 (1 mg X ml-1) onto the tracheal mucosa induced local Evans blue extravasation. This response was resistant to pretreatment with histamine receptor antagonists, but was largely inhibited after neonatal capsaicin pretreatment. Topical administration of compound 48/80 (1 mg X ml-1 or 10 mg X ml-1) into the eye did not cause visible Evans blue extravasation in the conjunctiva, nor any signs of pain reaction as indicated by the absence of the wiping response, usually seen upon noxious chemical stimuli in the eye. In guinea-pigs, 10 mg X kg-1 compound 48/80 i.v. were required to induce vascular protein leakage in different organs. This response was blocked by pretreatment with H1 and H2 receptor antagonists, but only slightly reduced after systemic capsaicin pretreatment of guinea-pigs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of compound 48/80--induced vascular protein leakage by pretreatment with capsaicin and a substance P antagonist. 608 60

The effects of substance P (SP), substance K (SK), physalaemin, eledoisin, kassinin, neuromedin K and bombesin on blood pressure, heart rate, respiratory insufflation pressure and plasma extravasation were studied in the guinea-pig. All tachykinins except neuromedin K caused a fall in blood pressure with rather similar potency. The hypotensive response after physalaemin was comparatively more long-lasting. SK and eledoisin (2.5 nmol X kg-1 i.v.) caused an initial bradycardia which then changed into tachycardia. The other tachykinins induced a slowly developing tachycardia. Neuromedin K (up to 40 nmol X kg-1) did not influence heart rate. SK, kassinin and eledoisin were more potent than SP and physalaemin in increasing respiratory insufflation pressure. The effect of SK had a particularly long duration. Neuromedin K only induced a weak increase in insufflation pressure at a very high dose. All tachykinins except neuromedin K induced an increase in vascular permeability to plasma proteins in many visceral organs, as indicated by Evans blue extravasation. The trachea and ureter were the most sensitive organs with regard to this effect. Physalaemin and eledoisin were generally more potent in increasing vascular permeability in various organs than SP and SK. The maximal permeability-increasing effect of SK was smaller than that of SP, although the potency was similar. Bombesin increased insufflation pressure with no clearcut effects on vascular permeability. It is concluded that in the same species, i.e. guinea-pig, several tachykinins have rather similar hypotensive action, while the vascular permeability increase to plasma proteins is especially pronounced after physalaemin and eledoisin. SK, kassinin and eledoisin have prominent bronchoconstrictor effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of cardiovascular and bronchoconstrictor effects of substance P, substance K and other tachykinins. 608 17

Substance P-immunoreactivity (SP-IR) in the guinea-pig ureter was found to be totally depleted after systemic capsaicin pretreatment. Removal of the inferior mesenteric ganglion (IMG) led to a total depletion of SP-IR from the rostral third of the ureter and to a partial depletion from the caudal third. Electrical stimulation of the IMG caused Evans blue extravasation mainly in the rostral third of both ureters, whereas stimulation of the right pelvic nerve caused Evans blue extravasation in the caudal third of the ureters on both sides. The responses to nerve stimulation were absent in capsaicin-pretreated animals. Furthermore, capsaicin caused release of SP-IR from ureter slices in vitro, this release was not inhibited by tetrodotoxin. Potassium (60 and 120 mM) also released SP-IR. It is concluded that SP-IR in the ureter is contained in capsaicin-sensitive sensory neurons reaching the ureter via both parasympathetic (caudal part) and sympathetic nerves (rostral part). Activation of these neurons by capsaicin leads to a peripheral release of SP-IR which most likely increases vascular permeability.
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PMID:Capsaicin-induced substance P release and sensory control of vascular permeability in the guinea-pig ureter. 619 95

The occurrence of neurogenic inflammation as indicated by Evans blue extravasation was studied in various organs of the guinea-pig. Electrical stimulation of the trigeminal nerve caused Evans blue extravasation due to increased vascular permeability in the nasal mucosa and gingiva. Vagal stimulation induced extravasation in the epiglottis, larynx, trachea, bronchial tree and esophagus. Splanchnic stimulation induced Evans blue extravasation in the gall bladder, bile ducts and superior mesenteric artery. Stimulation of the inferior mesenteric ganglion caused a marked extravasation in the upper and middle part of both ureters, while pelvic activation induced a reaction in the lower ureter, urinary bladder, urethra and vagina. I.v. substance P (SP) (3 nmol X kg11) or capsaicin (1 mumol X kg-1) both induced extravasation in many tissues including those in which nerve stimulation produced a response. The extravasation responses to SP, capsaicin or nerve stimulation all had similar border-line zones, such as esophagus to stomach, bile ducts to duodenum, rectum to anal mucosa, pulmonary artery to heart and vagina to uterus. Quantitative determinations showed especially large permeability effects in the trachea, umbilical ligament and ureter. The permeability effect of capsaicin and nerve stimulation was abolished in capsaicin-pretreated animals, while the response to SP was still present. Capsaicin pretreatment caused an almost total loss of SP in several visceral organs including the respiratory and urinary tracts. The SP content in these tissues was correlated (r = 0.97) to the Evans blue extravasation following nerve stimulation or i.v. capsaicin. SP and capsaicin caused contractions in vitro of the esophagus, ureter, urinary bladder, trachea and gall bladder. The capsaicin-induced contraction of the trachea was resistant to tetrodotoxin pretreatment. The non-cholinergic, non-adrenergic contraction of the urinary bladder upon field stimulation was still present in capsaicin-pretreated animals. In conclusion, neurogenic inflammation occurs in several organs with a highly region-specific distribution, which is accompanied by the presence of capsaicin-sensitive SP neurons. Both parasympathetic and sympathetic pathways contain capsaicin-sensitive afferent fibres which mediate an increase in vascular permeability most likely by releasing SP. In addition, both capsaicin and SP cause smooth muscle contraction in several visceral organs.
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PMID:Vascular permeability changes and smooth muscle contraction in relation to capsaicin-sensitive substance P afferents in the guinea-pig. 620 Oct 40

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

A 50-year-old woman with a 4-year history of Evans syndrome was admitted to our hospital because of progressive nausea, appetite loss, body weight loss, diarrhea and abdominal pain. Abdominal ultrasonography revealed pleural effusion, ascites, bilateral hydronephrosis, dilatation of the bilateral ureter, and irregular wall thickness of the urinary bladder. Immunological studies revealed decreased complement components (C3; 72 mg/dl, C4; 7 mg/dl, CH50; 28.8 mg/dl), a x 80 antinuclear antibody titer (homogeneous pattern), antibody against single-stranded DNA 19 U/ml, anti-SS-A antibody over 500 U/ml and negativity for antibody against double-stranded DNA (anti-dsDNA Ab). Although the patient did not fulfill the criteria for systemic lupus erythematosus (SLE), we diagnosed her as having lupus cystitis. Bolus methylprednisolone (mPSL) therapy (1,000 mg mPSL over 3 days, div) was administered, followed by 60 mg PSL, and this led to immediate improvement of the patient's symptoms and laboratory data. Later, anti-dsDNA Ab became positive, and the patient thereby fulfilled the criteria for SLE. Lupus cystitis following Evans syndrome has rarely been reported. The present such case was treated successfully with bolus mPSL therapy.
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PMID:[Lupus cystitis in the course of Evans syndrome]. 1186 59