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

A method has been proposed for the kinetic analysis of the relaxation phase of mechanical response of smooth muscle. The method implies linearization of the entire mechano-kinetic relaxation curve using the coordinates ln[(fm-f)/f]; ln t (where fm and f are the maximal and the actual values of force within the relaxation phase respectively) with subsequent calculation of the maximal amplitude--normalized relaxation rate, Vn. The use of the method is illustrated on ureter, protal vein, vas deferens, myometrium of rat and guinea-pig ureter smooth muscles in a variety of experimental conditions. This method can be applied for the description of the calcium transient decay in the myoplasm measured with Ca-sensitive fluorescent dyes. The method might be useful for identification of the contribution of different energy-dependent Ca-transporting systems involved in the control of relaxation, as well as for screening of the mechanisms of action of different factors which modulate the contraction-relaxation cycle.
Gen Physiol Biophys 1991 Dec
PMID:Kinetic analysis of smooth muscle relaxation. 180 80

The role of the electrogenic Na(+)-Ca(2+)-exchange mechanism in regulating the spike activity of the ureter was studied. The ureter cells were shown to be capable of generating action potentials (AP) in sodium-free Krebs solution. The time during which the spikes are generated is in exponential dependence on the concentration of calcium ions in the medium, [Ca2+]o within 2.5 to 15 mmol/l. Simultaneously with the generation of the spikes, accumulation of calcium in the muscles is observed, proportional to the increase of [Ca2+]o. The addition of as little as 20 mmol/l Na+ or Li+ ions into the solution restores the prolonged electrical activity of the ureter. Under these conditions, the decrease of intracellular Ca2+ within 5 min was more than two times larger as compared with that in sodium-free medium. Upon substituting Ba2+ ions for Ca2+ ions in Krebs solution AP are generated within an interval which was the longer the higher the Ba2+ concentration in the medium. Li+ ions can replace Na+ ions in maintaining AP and in extruding calcium from the cell. It is supposed that the generation of the stable spike activity of the ureter depends on the functioning of Na(+)-Ca(2+)-exchange mechanism.
Gen Physiol Biophys 1991 Apr
PMID:Factors controlling the intracellular concentration of calcium and the spontaneous activity of the ureter. 186 94

The effects of caffeine on the electrical and mechanical activity of the guinea-pig ureter smooth muscle were studied. Under untreated conditions caffeine mainly showed inhibitory action on the ureter, inhibiting the evoked action potentials and phasic contractions as well as potassium contracture. Caffeine was also found to suppress the low-Na contracture of Na-loaded ureter muscle. It is established that Na-loaded tissue is able to generate transient contracture in response to caffeine application at 37 degrees C. These caffeine contractures could be evoked under completely removed [Ca2+]0 and in the presence of high doses of Ca-channel blockers (nifedipine, diltiazem, Mn ions) and could be reversibly blocked by tetracaine, procaine and benzocaine. Caffeine contractures could also be produced by the ureter muscle placed in isotonic K-solution. Cooling significantly potentiated low-Na, potassium and caffeine contractures of the ureter muscle. Filling of the store is totally dependent on the entry of Ca ions from the extracellular Ca2+ store sites which sequester Ca ions entering the cell on either Na-Ca exchange or via voltage operated Ca channels.
Gen Physiol Biophys 1986 Dec
PMID:Effects of caffeine on the electrical and mechanical activity of guinea-pig ureter smooth muscle. 243 12

Effects of temperature and Na0+ on the relaxation of guinea-pig ureter smooth muscle were studied. Relaxation of phasic contraction was found to be highly temperature-dependent, practically independent of Na0+ and Ca02+, and resistant to vanadate. The relaxation of the tonic tension of both high-K and low-Na contracture was less temperature-dependent and affected by Na0+. The relaxation of tonic tension produced by introduction of Na0+ was about 3-5 times faster than that produced by Ca-free solution. La3+ ions were found to block the relaxation of the tonic component of the Na+-free contracture initiated by removal of Ca02+. Three systems of regulation of cell calcium are suggested to be operative in the ureter muscle: a fast one which is highly temperature-dependent and responsible for the relaxation of the phasic contraction (probably the sarcoplasmic reticulum), and two slow membrane-linked carriers, one of which is dependent on Na0+ (probably Na-Ca exchange) and another one which is independent of Na0+ and inhibited by La3+ (probably Ca-pump).
Gen Physiol Biophys 1988 Feb
PMID:Effects of temperature and Na0+ on the relaxation of phasic and tonic tension of guinea-pig ureter muscle. 339 48

The configuration of the electrotonic potential and the action potential observed by the double sucrose-gap method was similar to that observed with a microelectrode inserted into a cell in the center pool between the gaps. In the taenia and the ureter, the evoked spike was larger in low Na or in Na-free (sucrose substitute) solution than in normal solution. However, the plateau component in the ureter was suppressed in the absence of Na. In Ca-free solution containing Mg (3-5 mM) and Na (137 mM), the membrane potential and membrane resistance were normal, but no spike could be elicited in both the taenia and ureter. Replacement of Ca with Sr did not affect the spike in the taenia, nor the spike component of the ureter but prolonged the plateau component. The prolonged plateau disappeared on removal of Na, while repetitive spikes could still be evoked. It was concluded that the spike activity in the taenia and in the ureter of the guinea pig is due to Ca entry, that the plateau component in the ureter is due to an increase in the Na conductance of the membrane, and that both mechanisms, for the spike and for the plateau, are separately controlled by Ca bound in the membrane.
J Gen Physiol 1970 Feb
PMID:The action potential in the smooth muscle of the guinea pig taenia coli and ureter studied by the double sucrose-gap method. 541 76

The participation of Na+ in regulation of intracellular Ca++ content and in formation of spontaneous action potentials of guinea-pig ureter was studied. It was shown that the fast decrease of intracellular Ca++ in the Ca(++)-loaded muscles was accompanied by enhancement of Na+ content in the cells. The concentration gradient of Na+ was found to define the effectiveness of Ca(++)-extrusion from Ca(++)-loaded cells. The decrease of intracellular Ca++ showed a sigmoidal dependence on Na+ content in the medium. A correlation was established between the concentration gradient of Na+ and the formation of action potential plateau of ureter smooth muscle cells. The duration of action potential plateau decreased in accordance with Ca++ efflux and Na+ influx. The results confirmed the participation of Na(+)-Ca++ exchange mechanism in support of Ca++ cellular homeostasis as well as in the generation of action potentials of guinea-pig ureter.
Gen Physiol Biophys 1994 Dec
PMID:Na(+)-Ca++ exchange mechanism in smooth muscle of the ureter. 779 52

Effects of chlorpromazine, haloperidol (neuroleptics and calmodulin antagonists), and verapamil on rat platelet aggregation induced by thrombin, on calcium current in snail neurones and on both tonic tension of high potassium contracture and phasic contraction of isolated guinea-pig ureter preparations were studied. Moreover, droperidol, sulpiride and prazosine effects were studied for models of phasic contractility and platelet aggregation. Sulpiride and prazosine were ineffective, verapamil was ineffective on platelet aggregation, while droperidol was the most potent inhibitor of platelet aggregation. These results, the similarity revealed in the blockage of neuronal calcium current by neuroleptics and verapamil, and the potent inhibitory action of haloperidol and chlorpromazine on contractility and aggregation suggest that both phenothiazine and butyrophenone neuroleptics possess some properties of calcium antagonists and may also have intracellular sites of action other than calmodulin.
Gen Physiol Biophys 1995 Aug
PMID:Effects of haloperidol and chlorpromazine on smooth muscle contractility, platelet aggregation and neuronal calcium current. 872 Jun 98

1. In the guinea pig isolated ureter, a maximally effective concentration of calcitonin gene-related peptide (CGRP, 0.1 microM) produced a prompt and transient suppression of myogenic phasic contractions (twitches) evoked by direct excitation (electrical field stimulation, EFS) of the smooth muscle. This suppressant effect is prevented by glibenclamide (1 and 10 microM), indicating the importance of K+ channel activation in its genesis. In the presence of either 1 or 10 microM glibenclamide, CGRP produced a partial (about 30%) and delayed inhibition of the evoked response, but failed to produce a full suppression of twitches. 2. The intensity and duration of the early, glibenclamide-sensitive suppressant effect of CGRP were inversely related to the frequency at which the ureters were driven by EFS. The glibenclamide-resistant inhibitory effect of CGRP was unaffected by changes in the EFS driving frequency, and cromakalim (3 microM) suppressed twitches independently of the EFS driving frequency. 3. Replacement of 80% glucose in the Krebs solution with 2-deoxyglucose (2-DOG) reduced the amplitude of the EFS-evoked twitches. In the presence of 2-DOG the inhibitory effect of CGRP was enhanced and prolonged when tested in the absence, but not in the presence, of glibenclamide. 2-DOG counteracted the inhibitory effect produced by increasing the EFS driving frequency on the response to CGRP. 4. In sucrose gap, both CGRP (0.1 microM) and cromakalim (3 microM) produced prompt hyperpolarization of the membrane. During continued superfusion for 15 min in unstimulated preparations, the hyperpolarizing effect of cromakalim and CGRP was sustained. When tested within 3 min from the end of 'exercise', induced by application of EFS at intervals of 15 sec for 30 min, the hyperpolarization by CGRP was reduced and shortened but that produced by cromakalim was unaffected. 5. These findings demonstrate that exercise and metabolic inhibition selectively influence, in opposite directions, the K+ channel opener action of CGRP in the guinea pig ureter, indicating that the ability of this neuropeptide to suppress latent pacemakers in smooth muscle is markedly dependent upon degree/frequency of cell activation. These results suggest that the ability of endogenous CGRP to suppress ureteral motility may be inversely related to the frequency of ureteral peristalsis, the effect being reduced by, for example, increase in diuresis.
Gen Pharmacol 1996 Jan
PMID:Effect of exercise and 2-deoxyglucose on the K+ channel opener action of CGRP in the guinea pig ureter. 874 2

The first measurements of AVT-sensitive adenylate cyclase activity in specific segments of the nephron of the Australian arid-zone agamid lizard, Ctenophorus (=Amphibolurus) ornatus, are reported. All sections of the collecting-duct system of this lizard were found to be sensitive to AVT at a concentration of 1 x 10(-6) M. In addition, receptors to AVT were located in the thin-intermediate segment linking proximal and distal convoluted tubules. No significant response to AVT was detected in the glomeruli, in either proximal or distal convoluted tubules, or in the ureter. The physiological significance of these particular segments is discussed in terms of the action of AVT in stimulating water and salt reabsorption in the lizard kidney.
Gen Comp Endocrinol 1996 Sep
PMID:Arginine vasotocin: locus of action along the nephron of the ornate dragon lizard, Ctenophorus ornatus. 881 98

1. We have investigated the effect of various protein kinase A (PKA) inhibitors on the phasic and tonic components of the response to potassium chloride (KCl) in the guinea pig ureter. All experiments were performed in ureters pretreated with capsaicin (10 microM for 15 min) to prevent the release of sensory neuropeptides and in the presence of 1 microM Bay K 8644 to maximize calcium (Ca) entry via voltage-sensitive channels. The addition of 80 mM hypertonic KCl produced maximal shortening of the ureter with distinct phasic and tonic components, the latter further showing a transient and a sustained component. Nifedipine (30 microM for 120 min) totally abolished all the responses to KCl. 2. The selective PKA inhibitor, H89 (10 microM), abolished the tonic response to KCl in about 30 min with minor inhibitory effect on the phasic contraction. This pattern was unchanged when extending the contact time to 120 min. When added 30 min before the next challenge, H89 (1-30 microM) concentration-dependently inhibited the responses to KCl with a preferential inhibitory effect on the tonic contraction. Another PKA inhibitor, H8, produced similar effects at tenfold higher concentrations (10-300 microM) than H89, consistent with the known potency ratio of these isoquinoline derivatives in inhibiting PKA. 3. The potent and nonselective protein kinase inhibitor, staurosporine (10-100 nM) produced an even depression of the various phases of the response to KCl. The selective protein kinase G inhibitor, KT 5823 (10 microM for 60 min) produced only a slight reduction of the sustained tonic response to KCl. The selective protein kinase C inhibitor GF 109,203X (1-3 microM) and the cAMP analog, Rp-cAMPS (300 microM for 60 min) had no effect on the three components of the response to KCl. 4. In the presence of Bay K 8644, electrical field stimulation (10 Hz for 1 sec, 60 V, pulse width 5 ms) produces direct myogenic phasic contractions (twitches) of the ureter which are suppressed by nifedipine (10-30 microM). H8 (up to 30 microM) and H89 (up to 300 microM) had minor effect on the amplitude of twitches, consistent with their poor inhibitory activity on the phasic responses to KCl. 5. In sucrose gap, superfusion with 80 mM hypertonic KCl produced action potentials followed by a sustained depolarization of the membrane: the two electrical responses underlie the phasic and tonic components of contraction to KCl, respectively. H89 (10 microM for 30 min) did not affect the resting membrane potential nor the KCl-evoked action potentials and sustained depolarization. H89 had no effect on the phasic contraction to KCl but markedly depressed (about 65% inhibition) the tonic contraction. 6. The present findings are consistent with the view that phosphorylation by PKA increases the availability of L-type Ca channels in the ureter smooth muscle. Blockade of PKA dissociates the electromechanical coupling between the sustained membrane depolarization produced by KCl and the corresponding sustained increase in tension. The L-type Ca channel responsible for generating action potentials and phasic contractions to KCl are less sensitive to PKA inhibitors than those responsible for the tonic contraction.
Gen Pharmacol 1996 Mar
PMID:Protein kinase A inhibitors selectively inhibit the tonic contraction of the guinea pig ureter to high potassium. 891 54


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