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

1. Ionic currents underlying the action potential were recorded from enzymatically isolated smooth muscle cells of guinea-pig ureter. 2. The action potential recorded from a single cell was similar to that from a multicellular preparation. It showed repetitive spikes on a plateau potential which followed the first spike. Treatment with 10 mM-tetraethylammonium (TEA) increased the amplitude and duration of the plateau phase and abolished the repetitive spikes. 3. Under voltage clamp mode, at least two (maybe three) kinds of outward currents were activated during depolarizing pulses. The main outward current was Ca2+-dependent K+ current (IK(Ca], which was mostly blocked in Ca2+-free solution, or by application of 1 mM-cadmium (Cd2+) or 2 mM-tetraethylammonium (TEA). IK(Ca) was greatly decreased by treatment with 5 mM-caffeine or an addition of 10 mM-EGTA in a pipette solution. 4. In the presence of 1 mM-Cd2+ and 2 mM-TEA, a small transient outward current remained. 4-Aminopyridine (1 mM) suppressed the transient outward current by about 40%. Time- and voltage-dependent delayed rectifier outward currents were small in ureter cells. An inwardly rectifying K+ current was not detected. 5. An application of 1 mM-Cd2+, 5 mM-cobalt (Co2+), 1 mM-lanthanum (La3+) or 0.1 microM-nifedipine completely blocked the action potential. Replacement of 80-90% of extracellular Na+ with Li+ or Tris almost abolished the plateau potential and repetitive spikes but did not change significantly the first spike. 6. In the presence of 30 mM-TEA, the inward current elicited by depolarization was monophasic and lasted for more than 1 s. Application of 1 mM-Cd2+, 1 mM-La3+, 0.1 microM-nifedipine, or 5 mM-Co2+ completely blocked inward current. The replacement (87%) of extracellular Na+ ions with Li+, Tris, sucrose or TEA speeded up the decay of inward current; the inward current decreased by 10-60% at the end of a 500 ms pulse. 7. Even in low-Na+ solution (120 mM-TEA), the inactivation of ICa had a quite slow component (tau = 1 s), in addition to another faster component (tau = 100 ms) at 0 mV. When short depolarizing clamp pulses (50 ms) were repetitively applied at short intervals (50 ms) and with interpulse voltage of -10 or -20 mV to mimic the repetitive spikes on the plateau of the action potential, the decline of peak Ca2+ current during the train of pulses was smaller than the decay of Ca2+ current during a long pulse.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Ionic currents in single smooth muscle cells from the ureter of the guinea-pig. 248 52

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

The effects of various K(+) channel blockers on the spontaneous electrical activity of the smooth muscle cells of the ureter still attached to its primary pacemaker regions were investigated using standard intracellular microelectrode recording techniques. Spontaneous action potentials in the ureter were complex, consisting of an initial rapidly rising spike which was followed by a period of membrane oscillation, a quiescent plateau phase and terminated by an abrupt repolarisation and an after-hyperpolarisation with a peak "diastolic" potential of -66 mV. This after-hyperpolarization decayed slowly over 5-20 s until the underlying triggering potentials achieved threshold for another action potential discharge. Application of the Ca(2+)-entry blocker, nifedipine (1 mu;M), blocked action potential discharge within 2-5 min, after which the membrane settled at a potential of -55 mV. 4-Aminopyridine (4-AP)(1 mM for 2 min) and Ba(2+) (100 mu;M for 2 min) both depolarized significantly the diastolic potential. In 4-AP, this membrane depolarisation was associated with a decreased amplitude of the initial spike and an increase in the half-amplitude duration. In contrast, tetraethylammonium (TEA) (0.5 mM for 2 min) only increased the frequency and half-amplitude duration of these ureteric action potentials. Apamin (200 nM), Cs(+) (1 mM) and glibenclamide (1 microM) had no significant effects on any parameters of the ureteric action potential. It was concluded that the refractory period of the spontaneous action potentials in the whole-mount preparation of the upper urinary tract was determined by the opening of at least three K(+) channel populations: large conductance ('maxi K') Ca(2+)-activated K(+) channels; Ca(2+)-insensitive transiently opening K(+) (I(Kto)) channels and K(+)-selective inward rectifier channels.
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PMID:K(+) channel blocker modulation of the refractory period in spontaneously active guinea-pig ureters. 1055 May 19