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

Guinea pig's ureter rhythmogenic autonomous latent pacemaker was shown to generate a significantly higher-frequency rhythm than the pericystic pacemaker. The latent pacemakers of the ureter middle portion can be activated with a breach of electrical conductivity across the organ or with chemical agents (noradrenaline, histamine).
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PMID:[Activation of latent pacemakers in the guinea pig ureter]. 1157 29

1 This study was designed to investigate the effect of 5-hydroxytryptamine (5-HT) and to characterize the 5-HT receptors involved in 5-HT responses in the pig intravesical ureter. 2 5-HT (0.01-10 microM) concentration-dependently increased the tone of intravesical ureteral strips, whereas the increases in phasic contractions were concentration-independent. The 5-HT(2) receptor agonist alpha-methyl 5-HT, mimicked the effect on tone whereas weak or no response was obtained with 5-CT, 8-OH-DPAT, m-chlorophenylbiguanide and RS 67333, 5-HT(1), 5-HT(1A), 5-HT(3) and 5-HT(4) receptor agonists, respectively. 5-HT did not induce relaxation of U46619-contracted ureteral preparations. Pargyline (100 microM), a monoaminooxidase A/B activity inhibitor, produced leftward displacements of the concentration-response curves for 5-HT. 3 5-HT-induced tone was reduced by the 5-HT(2) and 5-HT(2A) receptor antagonists ritanserine (0.1 microM) and spiperone (0.2 microM), respectively. However, 5-HT contraction was not antagonized by cyanopindolol (2 microM), SDZ-SER 082 (1 microM), Y-25130 (1 microM) and GR 113808 (0.1 microM), which are respectively, 5-HT(1A/1B), 5-HT(2B/2C), 5-HT(3), and 5-HT(4) selective receptor antagonists. 4 Removal of the urothelium did not modify 5-HT-induced contractions. Blockade of neuronal voltage-activated sodium channels, alpha-adrenergic receptors and adrenergic neurotransmission with tetrodotoxin (1 microM), phentolamine (0.3 microM) and guanethidine (10 microM), respectively, reduced the contractions to 5-HT. However, physostigmine (1 microM), atropine (0.1 microM) and suramin (30 microM), inhibitors of cholinesterase activity, muscarinic- and purinergic P(2)-receptors, respectively, failed to modify the contractions to 5-HT. 5 These results suggest that 5-HT increases the tone of the pig intravesical ureter through 5-HT(2A) receptors located at the smooth muscle. Part of the 5-HT contraction is indirectly mediated via noradrenaline release from sympathetic nerves.
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PMID:Characterization of the 5-hydroxytryptamine receptors mediating contraction in the pig isolated intravesical ureter. 1252 83

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

High levels of various uremic toxins such as guanidino compounds and advanced glycation endproducts, as well as an excess of parathyroid hormones, are involved in the pathogenesis of acute uremic encephalopathy. Moreover, distant effects of the damaged kidney with enhanced production of inflammatory mediators are implicated. Data on the pump activity of an abnormal Na-K-ATPase and inhibition of the organic anion transporter system in the brain have been published previously. Recently, the effect of an experimentally induced acute renal failure (ARF) on the neuronal cell activation of Fos and Fra-2 in the rat brain was investigated by immunohistochemistry. ARF was induced by using the following 3 rat models: bilateral nephrectomy, bilateral ureter ligation, and uranyl acetate injection with corresponding controls. The Fos and the Fra-2 immunoreactive neurons of the brain were determined in a total of 120 brain areas over a period of 3 days post bilateral nephrectomy and bilateral ureter ligation and 12 days after uranyl acetate. An activation response was observed in 73 of 120 areas of the brain. The responses were classified into 4 groups: (1) biogenic amines (noradrenaline, adrenaline, histamine, and 5-hydroxytryptamine), (2) stress-sensitive forebrain areas, (3) neuronal cell groups involved in the regulation of water and electrolyte homeostasis, and (4) central autonomic cell groups. In the uranyl acetate-induced ARF, activation of Fos and Fra-2 immunoreactivity took place at the earliest time-point (3 hours) which persisted even after improvement of ARF. This suggests the involvement of the toxic effects of uranium as a result of its accumulation in the brain.
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PMID:Mechanisms of acute uremic encephalopathy: early activation of Fos and Fra-2 gene products in different nuclei/areas of the rat brain. 2079 70


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