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 verapamil, a calcium antagonist agent, were studied on smooth muscle preparations of the lower urinary tract of horses. Verapamil (2 X 10(-4) to 2 X 10(-8) M) relaxed the ureter, urethra and urinary bladder preparations contracted by potassium (127 mM), L-noradrenaline (2 X 10(-5) M), histamine (2 X 10(-5) M) and acetylcholine (2 X 10(-5) M). These results allow the conclusion that verapamil has a dose-dependent relaxing effect on smooth muscle of the lower urinary tract.
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PMID:Effects of verapamil on the smooth muscle of the horse urinary tract. 408 36

1. The relation between density of adrenergic innervation, noradrenaline (NA) accumulation (as seen with the fluorescence histochemical method) in tissues incubated in a high concentration of NA, and monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) activities, were examined in a wide range of tissues from different species.2. Evidence was obtained to support the proposal that accumulation of NA in the non-innervated smooth muscle of the human umbilical artery and chick amnion is associated with very low activities of COMT within muscle cells.3. The wide variation in tissue accumulation of NA in adrenergically innervated muscles was confirmed. For example, in the rabbit atrium and rat vas deferens, there was high NA accumulation in vascular smooth muscle but not in other muscle cells. In the mouse vas deferens there appeared to be preferential NA accumulation in the outer longitudinal muscle in comparison with the circular muscle. In the ventricle of the rat and mouse individual muscle cells showed different degrees of accumulation of NA. Many unidentified fluorescent cells were revealed in the submucosa of the guinea-pig ureter following loading with NA. The highest activities of COMT were found in the rat vas deferens and the lowest in the rabbit vascular tissues; the highest activity of MAO was found in the guinea-pig ileum, and the lowest in the rat aorta.4. No simple relation between tissue activities of MAO and COMT and degree of NA accumulation was found. Possible directions for further investigation of the problem are discussed.
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PMID:Factors affecting the extraneuronal inactivation of noradrenaline in cardiac and smooth muscle. 467 48

1. A method of recording the peristaltic frequency and the rate of transport of fluid (perfusion rate) in the rat ureter in vivo is described.2. Acetylcholine and atropine did not alter ureteral activity. Histamine increased the rate of peristalsis by up to 15% and the rate of perfusion by up to 10%. Low doses of 5-hydroxytryptamine increased peristaltic frequency whereas high doses decreased peristaltic frequency; all doses reduced the rate of perfusion.3. Morphine reduced the rate of perfusion by 5-10% at all dose levels, but only the highest dose used reduced the frequency of ureteral peristalsis.4. (-)-Adrenaline, (-)-noradrenaline and (+/-)-isoprenaline reduced the frequency of peristalsis. The order of potency was isoprenaline>noradrenaline>adrenaline. The response was dose-related and blocked by propranolol, which itself did not affect ureteral activity.
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PMID:The pharmacology of the rat ureter in vivo. 504 47

1 The concept that presynaptic receptors regulate noradrenergic transmitter release via a system of inhibitory receptors mediating negative feedback relies on a supposed association between increases in stimulation-induced efflux of [3H]-noradrenaline by antagonists and blockade by them of the inhibitory effects of exogenous noradrenaline. 2 It was shown in guinea-pig ureter, that yohimbine (3 X 10(-7)M), a presumed selective presynaptic antagonist, increased transmitter efflux substantially at 1 Hz and 5 Hz with 100 pulses, purportedly representing antagonism of the inhibitory effect of locally released noradrenaline but did not reduce the inhibitory effect of exogenous noradrenaline (1.8 X 10(-6)M or 1.8 X 10(-7)M) except in one case. 3 Additionally, the inhibitory effect of oxymetazoline (1.0 X 10(-7)M or 1.0 X 10(-8)M) on stimulation-induced efflux was in no way antagonized by yohimbine (3 X 10(-7)M). 4 It is concluded that the increased efflux of [3H]-noradrenaline produced by antagonists and the decreased efflux produced by exogenous agonists may represent actions at different loci and that the hypothesis of presynaptic feedback regulatory sites is still not substantiated.
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PMID:Evidence against the unitary hypothesis of agonist and antagonist action at presynaptic adrenoceptors. 612 40

In vivo pacemaker potentials of canine renal pelvis were able to be recorded by our new method. Potentials recorded at the pelvicalyceal region of canine renal pelvis in vivo had two phasic slow rising wave form that had duration of 0.2 sec, amplitude of 20 microV and discharge interval of about 5 sec. Furthermore, the discharge interval of ureter EMGs was a integral multiple of that of pacemaker potentials. In diuretic state by intravenous administration of furosemide, pacemaker potentials showed no change in wave form and discharge interval. However, ureter EMGs occurred more frequently to correspond to pacemaker potentials one to one. Noradrenaline and isoproterenol had no action on pacemaker potentials. To the contrary, ureter EMGs were increased by noradrenaline and were decreased by isoproterenol. Acetylcholine had a great variety of action on both pacemaker potentials and ureter EMGs. These results suggest that the pelvicalyceal region as thought to be the pacemaker of ureteral peristalsis is controlled under the influence of parasympathetic nerve system and the ureter is controlled under the influence of both sympathetic and parasympathetic nerve systems.
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PMID:[Studies on the in vivo pacemaker potentials of the canine renal pelvis]. 652 Nov 27

Many workers have reported that alpha-adrenergic drugs activate and beta-adrenergic drugs suppress the ureteral activity. On the other hand, recent studies have proved that the pacemaker in the renal pelvis controls the ureteral peristalsis. In this study, in vivo and in vitro experiments were performed to explore the effects of autonomic drugs on pelvic pacemaker controlling the ureteral peristalsis. It was suggested that both of noradrenaline and isoproterenol stimulated the pacemaker activity itself, the former, however, elevated the renal pelvic pressure to accelerate the propagation of pacemaker activity consequently, while the latter decreased the renal pelvic pressure to suppress the propagation consequently. Acetylcholine stimulated the pacemaker activity and its propagation transiently, but base line of renal pelvic pressure with increased contraction pressure was decreased after drug administration. Furthermore, acetylcholine sometimes developed the retrograde peristaltic contraction from ureter to pacemaker region though the pelviureteral junction. Then acetylcholine might affect directly on ureter rather than on pacemaker itself and its propagation.
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PMID:[Experimental and physiological study on the effects of autonomic drugs upon the pacemaker activity of pelviureteral peristalsis]. 666 35

The action potential of human ureter was recorded in vitro by sucrose gap technique and the effects of some cations and drugs were studied. The action potential was composed of an initial fast component of spike and a subsequent slow component, a plateau, without a definite after-positive potential. Duration of the action potential was 1.0 +/- 0.1 (mean +/- standard deviation, n = 5) seconds at resting membrane potential level and 0.8 +/- 0.1 seconds at 90 per cent of the repolarization level. Ratio of plateau potential to spike potential was 80 +/- 4 per cent. The results of ionic influence suggested that calcium played an important role in the generation of spike potential and sodium in the generation of plateau potential. The application of noradrenaline and serotonin showed an excitatory effect which was observed as an increase of spontaneous discharge with depolarization of membrane potential and slow depolarization preceding the action potential. The slow depolarization was never observed in control preparations. These findings suggested that the ureter might have the capacity to generate a pacemaker-like slow depolarization which could conceivably relate to the automaticity of the ureter. Acetylcholine showed an excitatory effect only when the preparation was pretreated by physostigmine.
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PMID:Action potential of isolated human ureter recorded with sucrose gap technique. 683 25

1. The effects of papaverine (10(-5)-2 X 10(-4) M) were studied on the evoked electrical and mechanical activity of the guinea-pig ureter smooth muscle. In normal conditions the action potential consists of an initial spike followed by further spikes superimposed on a plateau phase. Papaverine reversibly decreased the duration of the plateau of the action potential, blocked the associated spikes, greatly reduced the amplitude of the contraction but enhanced the initial component of the action potential. 2. Papaverine did not change the membrane potential and had little effect on the membrane resistance. 3. Tetraethylammonium (5 mM), which blocks the delayed outward K current, did not prevent the decrease in the duration of the plateau nor the decrease of the contractile response caused by papaverine. 4. In Na-free solution the duration of the action potential was decreased until only a single spike was seen, due to suppression of the plateau. An effect of papaverine could not be observed under these conditions. 5. Mn2+ ions (1 mM) completely suppressed the spike component and tension while the plateau component was substantially increased. Papaverine in the presence of Mn2+ reversibly blocked the generation of the action potential. When Mn2+ ions were added to Na-free solution the duration as well as the amplitude of the spike was increased. Again, papaverine reversibly blocked the generation of the action potential. 6. Noradrenaline (10(-4) M) and histamine (10(-5) M) in normal conditions prolonged the duration of the action potential plateau and increased both the duration and amplitude of the concentration. Papaverine again blocked the plateau and greatly reduced the contractile response. 7. Papaverine caused the relaxation of KCl-induced contractures, preferentially blocking the tonic component. 8. It is suggested that the inhibitory action of papaverine on ureter smooth muscle results from its specific blockade of the 'slow' Na/Ca channels responsible for the generation of the plateau component of the action potential.
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PMID:The effects of papaverine on the electrical and mechanical activity of the guinea-pig ureter. 686 69

The conduction velocity of peristaltic movements of the canine ureter was measured under anaesthesia with a new type of diameter gauge using an image sensor. The peristaltic velocity was 34.1 +/- 6.2 mm/sec in 10 experiments. Noradrenaline at a low dosage of 1 microgram/kg i.v. reduced the resting diameter, increased the conduction velocity to 47--56 mm/sec, and approximately doubled the frequency of contraction. The application of acetylcholine also caused an increase in both frequency and conduction velocity (42--46 mm/sec). A plot of the conduction velocity against the mean period of peristaltic contraction was hyperbolic in shape.
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PMID:Conduction velocity of peristaltic waves in the in vivo ureter: application of a new diameter gauge. 723 14

1. The effects of noradrenaline (NA) on action potential shape and underlying membrane currents were examined in single smooth muscle cells freshly isolated from the ureter of the guinea-pig. 2. The voltage-dependent Ca2+ current (ICa) elicited upon depolarization from -50 to 0 mV was reduced by 27% upon application of 10 microM NA. This reduction was inhibited or converted to potentiation by internal application of low molecular weight heparin or 5 mM EGTA, indicating that it may be mediated by Ca(2+)-dependent Ca2+ channel inactivation via inositol 1,4,5-trisphosphate production and subsequent Ca2+ release from intracellular Ca2+ storage sites. 3. In contrast, Ba2+ current (IBa) through Ca2+ channels was potentiated by 36% in the presence of 10 microM NA. Internal application of GTP gamma S made it difficult to remove potentiation of IBa by wash-out; internal application of GDP beta S abolished potentiation. 4. NA caused a greater reduction in the transient Ca(2+)-dependent K+ current (IK(Ca)) upon depolarization than it did in ICa. This reduction was inhibited by internally applied heparin, suggesting that the amount of releasable Ca2+ in the storage sites was markedly reduced in the presence of NA. The sustained component of IK(Ca) which gradually increased during depolarization was also reduced by NA. 5. Action potential duration, which was recorded in a standard solution containing Ca2+, was prolonged by the application of NA. 6. It can be concluded that Ca2+ channel activity in ureter smooth muscle cells is regulated by a dual mechanism: Ca(2+)-dependent inhibition and GTP-binding protein-mediated potentiation. Under physiological conditions, both ICa and IK(Ca) were reduced by NA but the reduction of IK(Ca) was much larger than that of ICa; this results in an increase in net inward current during the action potential plateau and prolongs the action potential.
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PMID:Effects of noradrenaline on membrane currents and action potential shape in smooth muscle cells from guinea-pig ureter. 770 30


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