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

1. The ionic mechanism of the excitatory action of catecholamines and histamine on the smooth muscle cells of guinea-pig ureter was studied with the double sucrose-gap method. 2. In normal conditions adrenaline and noradrenaline in a concentration of 10(-5) g/ml., and histamine in a concentration of 10(-6) g/ml., prolonged the duration of the plateau of the action potential and increased the amplitude and duration of the phasic contraction. Sometimes these changes were accompanied by a slight depolarization of the muscle membrane and by a small increase (with noradrenaline) or decrease (with histamine) of the membrane resistance. The amplitude and duration of the fast spike component of the action potential were not changed. 3. Isoprenaline in a concentration of 10(-5) g/ml. either caused no change or it decreased the duration of the plateau, reduced the amplitude of contractions and reduced excitability. 4. Tetraethyl ammonium (TEA; 5 mM), which blocks the delayed outward K current, did not prevent the increase in the duration of the plateau nor the increase of the amplitude and duration of the contractions by noradrenaline and histamine. 5. In Na-free or in K-free solution or in the presence of ouabain, i.e. in conditions in which the Na-gradient across the membrane was reduced, noradrenaline and histamine were unable to increase the duration of the plateau and the amplitude and duration of the contraction. 6. In the presence of Mn2+ (2 mM) which suppressed the spike component of tha action potential and the phasic contraction, theeffects of noradrenaline and histamine were almost abolished. 7. The results suggest a dual ionic mechanism of the alpha-action of catecholamines and of the action of histamine on the smooth muscle of ureter: (1) these drugs affect the passive ionic permeability of the membrane in a manner that results in depolarization; (2) they specifically activate the potential-dependent conductance of the slow Na channels, thereby increasing the plateau duration. The increased amplitude and duration of the contraction is the result of their primary effect on the plateau of the action potential.
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PMID:The mechanism of the excitatory action of catecholamines and histamine on the smooth muscle of guinea-pig ureter. 84 27

Dogs were made azotemic by bilateral ureteral-venous anastomosis. Subsequently, the left ureter, a systemic artery, and the left renal vein were cannulated. Left renal blood flow (RBF) was measured by an electromagnetic flowmeter. Left renal clearances and extractions of [14C]tetraethylammonium ([14C]TEA) and p-aminohippuric acid (PAH) were determined at five 40-min intervals after administraiton of loading doses and institution of a maintenance infusion containing PAH and [14C]TEA. The renal extraction of TEA was independent of blood urea nitrogen (BUN), whereas the extraction of PAH correlated inversely with BUN. Renal plasma flows calculated from urinary clearances and renal extractions agreed with renal plasma flows calculated from flowmeter data. The extraction of TEA remained constant over the 200-min experimental period, whereas the extraction of PAH increases progressively as a function of time. It is probable that those organic acids which accumulate in azotemia, and interfered with renal tubular secretion of PAH, were themselves eliminated after opening the ureteral-venous anastomosis. Thus, TEA is superior to PAH for evaluation of the renal circulation in azotemia.
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PMID:Effects of azotemia on renal extraction and clearance of PAH and TEA. 126 21

Experiments were carried out on smooth muscle cells (SMC) of the guinea-pig ureter by the double sucrose gap method with simultaneous recording of electrical and contractile activities. The effect of histamine on SMC was studied in normal Krebs solution and in sodium-free Krebs solution with TEA. In normal Krebs solution, histamine was shown to increase the duration of AP plateau and contraction. In sodium-free Krebs solution with TEA, the APs of ureter SMC also had a plateau that was determined by the increased calcium conduction of the membrane. In these conditions, histamine provoked a decrease in the duration of the AP plateau and contraction. The histamine effect was blocked by phencarol both in normal and sodium-free Krebs solution with TEA. A possible role of sodium, calcium and potassium ions in the modulating action of histamine on excitation of ureter SMC is discussed.
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PMID:[Mechanism of modulating effect of histamine on the excitation and contraction of smooth muscles of the ureter]. 717 28

1. We have investigated the effect of the potassium (K) channel opener, cromakalim, on the spontaneous myogenic activity of the guinea-pig isolated renal pelvis and on myogenic contractions evoked by direct electrical stimulation of the guinea-pig isolated ureter. 2. In the presence of Bay K 8644 (1 microM), electrical stimulation of the guinea-pig ureter (10 Hz for 1 s, pulse width 5 ms, 60 V) produced regular tetrodotoxin-(1 microM) resistant phasic contractions which were suppressed by 3 microM cromakalim. Glibenclamide (0.1-3 microM), 4-aminopyridine (4-AP, 0.1-2 mM) and tetraethylammonium (TEA, 1-10 mM) produced a concentration-dependent inhibition of the effect of cromakalim with the rank order of potency (EC50 in parentheses): glibenclamide (0.64 microM) >> 4-AP (1.11 mM) > TEA (6.6 mM). Apamin (0.1-0.3 microM) was without effect. 3. Cromakalim (0.1-10 microM) produced concentration-dependent inhibition and suppression of spontaneous contractions of the guinea-pig isolated renal pelvis and of evoked contractions of the ureter with EC50 values of 0.71 and 0.47 microM, respectively. 4. Glibenclamide (1 microM) produced a rightward shift of the concentration-response curve to cromakalim in both the renal pelvis and ureter, without producing depression of the maximal inhibitory effect. Glibenclamide did not affect the spontaneous activity of the renal pelvis while it produced a slight enhancement (10-15% increase) of evoked contractions of the ureter. Glibenclamide did not affect the inhibitory action of the adenylate cyclase activator, forskolin, in the renal pelvis or ureter. 5. In electrophysiological experiments (sucrose gap), cromakalim (0.3 and 1 microM) produced hyperpolarization of ureter smooth muscle. Cromakalim also produced a transient suppression of action potentials and accompanying phasic contractions evoked by electrical stimulation. Before suppression of evoked contractions, a shortening of action potential duration was observed concomitant with the developing hyperpolarization produced by cromakalim. A lower concentration (0.1 MicroM) of cromakalim did not affect membrane potential but shortened action potential duration and reduced the evoked contraction.6. Glibenclamide (1 MicroM) inhibited the hyperpolarizing action of cromakalim and prevented its inhibitory action on evoked action potentials and contractions of the ureter. Glibenclamide also produced a slight prolongation of action potential duration and increased the amplitude and duration of the accompanying mechanical response.7. These findings demonstrate that activation of cromakalim- and glibenclamide-sensitive K channels produces a powerful mechanism for regulation of pyeloureteral motility and suppression of latent pacemakers of the ureter in guinea-pig. Glibenclamide-sensitive K channels take part in determining action potential shape and duration in the guinea-pig ureter.
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PMID:Effect of cromakalim and glibenclamide on spontaneous and evoked motility of the guinea-pig isolated renal pelvis and ureter. 801 47

Recent data have shown Ca(2+)-dependent activation of Rho-kinase by sustained depolarization of arterial smooth muscle. Visceral smooth muscles, however, contract phasically in response to action potentials and it is unclear whether Ca(2+)-dependent or -independent Rho-kinase activation occurs. We have therefore investigated this, under physiologically relevant conditions, in intact ureter. Action potentials, ionic currents, Ca(2+) transients, myosin light chain (MLC) phosphorylation and phasic contraction evoked by action potentials in guinea-pig and rat ureter were investigated. In rat, but not guinea-pig ureter, three Rho-kinase inhibitors, Y-27632, HA-1077 and H-1152, significantly decreased phasic contractions and Ca(2+) transients. Voltage- and current-clamp data showed that Rho-kinase inhibition reduced the plateau component of the action potential, inhibited Ca(2+)-channels and, indirectly, Ca(2+)-activated Cl(-) channels. The Ca(2+) channel agonist Bay K8644 could reverse these effects. The K(+) channel blocker TEA could also reverse the inhibitory effect of Y-27632 on the action potential and Ca(2+) transient. Ca(2+) transients and inward current, activated by carbachol-induced sarcoplasmic reticulum Ca(2+)release, were not affected by Rho-kinase inhibition. Rho-kinase inhibition produced a Ca(2+)-independent increase in the relaxation rate of contraction, associated with acceleration of MLC dephosphorylation, which was sensitive to calyculin A. These data show for the first time that: (1) Rho-kinase has major effects on Ca(2+) signalling associated with the action potential, (2) this effect is species dependent and (3) Rho-kinase controls relaxation of phasic contraction of myogenic origin. Thus Rho-kinase can modulate phasic smooth muscle in the absence of agonist, and the mechanisms are both Ca(2+)-dependent, involving ion channels, and Ca(2+)-independent, involving MLC phosphorylation activity.
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PMID:Rho-kinase inhibition and electromechanical coupling in rat and guinea-pig ureter smooth muscle: Ca2+-dependent and -independent mechanisms. 1533 77