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 autonomic receptor functions of ureteral smooth muscle were studied in vitro on strips of human ureter obtained at surgery. A dose-dependent, reproducible, contraction response to 5-hydroxytryptamine (Serotonin, 5-HT) was demonstrated. This response could be blocked by methysergide. Responses to acetylcholine and to drugs stimulating adrenergic receptor functions were also found, but they were weak and inconsistent. This suggests that contraction of ureteral smooth muscle is mediated through receptors which are sensitive to 5-hydroxytryptamine.
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PMID:Autonomic receptor functions of the human ureter: an in vitro study. 20 92

The influence of serotonin (5-hydroxytryptamine, 5-HT) on human ureteral smooth muscle was explored in a series of in vitro experiments. 5-HT evoked a dose-dependent contraction of the ureter. The effect of 5-HT was unaltered by blockade of 5HT3 and 5HT4 receptors and muscarinic cholinergic receptors. The 5HT2 receptor antagonist ketanserin (KT; 10(-5)-10(-4) M) and mixed 5HT1/5HT2 receptor antagonist methysergide (MS; 5 x 10(-5) M) inhibited the effect of 5-HT. Since the antagonist dissociation constant at 5HT2 receptors for both KT and MS is found to be approximately 10(-9) M, it is concluded that this contractile effect may have been mediated by some other, as yet uncharacterized 5-HT receptor. We believe that 5-HT is a potential neurotransmitter in the human upper ureteral smooth muscle.
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PMID:Influence of serotonin on the human ureter: an in vitro pharmacological study. 858 66

We investigated the effects of histamine on the motility of isolated segments from canine ureters and characterized pharmacologically the histamine receptors involved. We also evaluated the effects of various autacoids (5-HT, carbachol, noradrenaline, thromboxane, prostaglandin F2alpha) on the motility of canine ureters. Histamine as well as the H1 receptor agonist 2-(2-pyridyl)ethylamine elicited a concentration-dependent contraction. This contractile response was antagonized by dimethindene, causing a rightward shift (pA2 8.30) and a reduction of the slope and the maximal effect (pD'2 6.01) of the concentration-response curve. The histamine H2 receptor antagonist cimetidine in a concentration of 10(-5) mol/l was ineffective concerning the concentration-response curve for histamine. After precontraction of the ureter segments (5-HT, carbachol, prostaglandin F2alpha), a concentration-dependent relaxant effect was evaluated in the presence of histamine or the histamine H2 receptor agonist impromidine. The histamine H2 receptor antagonist cimetidine attenuated the relaxant response, causing a rightward shift of the concentration-response curve. All autacoids except thromboxane were capable of increasing contractility in canine ureters. Comparing the absolute contractile force in the presence of prostaglandin F2alpha, 5-HT, carbachol, noradrenaline and potassium, we found that histamine exhibits the most marked effect on this parameter in the canine ureter. It is concluded that there are two types of histamine receptors modulating contractile activity in the canine ureter: histamine H1 receptors, which mediate contraction, and histamine H2 receptors, which mediate relaxation (in the precontracted tissue).
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PMID:Characterization of histamine receptors in the ureter of the dog. 901 30

5-Hydroxytryptamine (5-HT) induced concentration-dependent contractions in human isolated ureteral strips in vivo. On the basis of available selective 5-HT agonists and antagonists, we have further investigated the receptors involved. At concentrations from 10 n m to 1 m m, 5-HT induced concentration-dependent contractions. Significant contractions were not observed with 5-HT1Aagonist 8-OH-DPAT (10(-9)-10(-4)m), 5-HT1Dalphaagonist sumatriptan (10(-9)-10(-4)m), 5-HT2agonist DOI (10(-9)-10(-4)m), 5-HT3agonist 2-methyl 5-HT (10(-9)-10(-3)m) and 5-HT4agonist renzapride (10(-9)-10(-3)m) on the human isolated ureter. On the other side, a 5-HT1-likeagonist 5-CT (10(-9)-10(-3)m) produced contractions on the isolated samples. The Emaxdeveloped by 5-CT was significantly smaller than that of the 5-HT (29% of 5-HT). Methithepin, the less selective 5-HT1/2antagonist (10(-9)-10(-6)m), 5-HT3antagonist, ondansetron (10(-9)-10(-5)m) and 5-HT4antagonist DAU 6285 (10(-8)-10(-6)m) did not antagonise the contractile responses to 5-HT. 10(-7)m ketanserin antagonised 5-HT induced contractile responses in ureteral strips. Additionally, combined administration of 5-HT4antagonist DAU 6285 (10(-6)m) and 5-HT1/2antagonist methithepin (10(-6)m) caused a rightward shift of the CRC of 5-HT yielding pEC50values of 4.68+/-0.15. 5-HT-induced contractile responses that were not abolished by TTX and atropine, thus supporting the suggestion that in the human, the contractile responses to cumulative addition of 5-HT of the ureter are not mediated by excitation of cholinergic neurons. In the present study the receptor mediating the contractile response to 5-HT in the human upper ureter could not be clearly designated 5-HT1-like, 5-HT2, 5-HT3or 5-HT4. This study suggests that contractile response to 5-HT in the upper segments of the human ureter appear to be mediated by an atypical 5-HT receptor subtype.
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PMID:Pharmacological analysis of 5-hydroxytryptamine effects on human isolated ureter. 1037 45

Non-steroidal anti-inflammatory drugs (NSAIDs) are currently considered a first-line treatment of renal colic. Their action has been ascribed to the inhibition of renal prostaglandin synthesis, which decreases renal blood flow and diuresis, and consequently lowers the pressure in the renal pelvis and ureter. However, the effects of NSAIDs on induced contractions of ureteral smooth muscle have received little attention. Also, there is a lack of clinically relevant spasmolytic drugs for the ureter. Therefore, we studied the influence of the non-selective cyclooxygenase (COX) inhibitor diclofenac, a NSAID drug customarily used in the treatment of renal colic, and of NS-398, a selective COX-2 inhibitor, on induced contractions of the pig ureter. Serotonin (0.1-30 microM), norepinephrine (0.1-30 microM) and neurokinin A (0.03-10 microM) induced reproducible concentration-dependent contractions, which were inhibited by diclofenac and NS-398 (10-300 microM) in a concentration-dependent manner. The sensitivity of neurokinin A-induced contractions to diclofenac was 3-4 times greater than that of the amines. Depending on the concentration, inhibition ranged between 25 and 96% of the initially induced contractile activity. In the presence of inhibitors, supramaximal concentrations of agonists were unable to trigger recuperation of the initially induced contractions. Prostaglandin F2alpha did not reverse the effect of diclofenac on agonist-induced contractions. Removal of diclofenac or NS-398 from the organ baths showed that the inhibition was totally reversible. Thus, the non-selective COX inhibitor diclofenac and the selective COX-2 inhibitor NS-398 are almost equipotent in reducing agonist-induced contractions in the isolated porcine ureter. Although the clinical relevance of this spasmolytic effect remains to be demonstrated, the data suggest that patients suffering from renal colic may benefit not only from the anti-diuretic and analgesic effects of diclofenac, but also from its potential spasmolytic properties. Moreover, selective COX-2 inhibitors may have clinical potential, as they may cause fewer side effects.
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PMID:Diclofenac and NS-398, a selective cyclooxygenase-2 inhibitor, decrease agonist-induced contractions of the pig isolated ureter. 1122 16

The effect of experimentally induced acute renal failure (ARF) on neuronal cell activation was investigated by immunohistochemistry for Fos and Fra-2 in the rat brain. ARF in rats was induced by bilateral nephrectomy (BNX), bilateral ureter ligature (BUL) and uranyl acetate injection with proper controls (sham-operation or saline injections, respectively). To follow the effect of the development of ARF, rats were killed 30 and 60 min, and 3, 12, 24 and 72 h after surgery, or 3 h to 12 days after uranyl acetate injections. In the BUL and BNX rats, urea and creatinine rose markedly in the plasma within 72 h, while in the uranyl acetate-injected rats the highest levels were observed on the 7th day, followed by a marked decline. At each time-point of the three different, experimentally induced ARF, the presence of Fos- and/or Fra-2-immunoreactive neurons was determined in 120 different brain areas and nuclei. In general, the 73 of 120 brain areas that showed time and intensity dependent activation in response to ARF can be classified into four groups: 1) biogenic amine (noradrenaline, adrenaline, histamine and 5-HT) expressing cell groups in the lower brainstem, 2) "stress-sensitive" forebrain areas, with regard to certain hypothalamic, limbic and cortical areas, 3) neuronal cell groups that participate in the central regulation of body and brain water and electrolyte homeostasis, including the circumventricular organs, and 4) central autonomic cell groups, especially visceral sensory cell groups in the brain, which are in primary, secondary or tertiary connections with renal afferents. Data presented here indicate that a wide variety of neurons in several regulatory mechanisms is affected by ARF-induced peripheral and central alterations.
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PMID:Neuronal activation in the CNS during different forms of acute renal failure in rats. 1917 83

Seizure associated with antiemetics is rare. We report seizure associated with a 5-HT(3) receptor antagonist in a 38 years old female. The patient underwent ureterorenoscopic lithotripsy due to left upper ureter stone. After operation, the patient complained of nausea in the postanesthetic recovery unit. In order to subside symptom, the patient was administrated 5-HT(3) receptor antagonist, palonosetron, 0.075 mg intravenously. Shortly after administration of that, the patient developed generalized tonic-clonic seizures. The symptom was subsided after midazolam and thiopental sodium were injected. But 40 minutes later, seizure recurred and subsided with midazolam again. The patient recovered completely without any specific sequelae.
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PMID:Seizure developed after palonosetron intravenous injection during recovery from general anesthesia -A case report-. 2294 88