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

Smooth muscle preparations of the urethra, bladder, and ureter were obtained from patients undergoing operations for various urological disorders. The urethral preparations were contracted by noradrenaline (0.1-3 microgram . ml-1), prostaglandin F2alpha (1-10 microgram . ml-1), and potassium (127 mM), the bladder preparations by carbacholine (0.004-1 microgram . ml-1), prostaglandin F2alpha (1-10 microgram . ml-1), potassium (127 mM), and barium chloride (3 mM), and the ureter preparations by potassium (127 mM), and barium chloride (3 mM). Irrespective of the mode of activation, pretreatment with nifedipine (0.1 microgram . ml-1) for 10 min. reduced the responses. Nifedipine also relaxed preparations contracted by the contractile agents used. In 19 female patients, aged 20 to 73 years, undergoing investigation because of urgency and/or urge incontinence, simultaneous urethrocystometry at rest was performed before and after oral administration of 20 to 40 mg nifedipine. Bladder capacity and residual urine were also determined. Nifedipine did not affect the pressures within the bladder and urethra, nor did it increase the bladder capacity. However, after nifedipine intake there was a statistically significant increase in residual urine. The results suggest that nifedipine can inhibit contractile activity induced by drugs with different modes of action; the drug does not affect the tone in bladder and urethra.
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PMID:Effects of nifedipine on the smooth muscle of the human urinary tract in vitro and in vivo. 69 40

Pain from ureteral stones is believed to be due to spasm and hyper-peristalsis of the involved ureter. Nifedipine has been shown to decrease human ureteral spasm in vitro. Conflicting results have been reported concerning the clinical efficacy of nifedipine in relieving acute renal colic. This prospective, double-blind, crossover clinical trial evaluated the acute pain relief obtained in 30 patients who had ureteral stones. All patients had ureteral stones documented either by plain abdominal radiograph (six), intravenous pyelogram (16), or passage of the stone(s) in the urine (eight). Each patient served as his own control. The mean pain relief scores for placebo versus 10 to 20 mg oral nifedipine were 0.7 +/- 1.8 and 1.2 +/- 2.5, respectively, as measured on a visual analogue scale (P = .404). Seven patients received clinically significant relief associated with nifedipine, and three patients received relief from placebo (P = .300). Twenty patients (66%) did not experience clinically significant relief from either treatment. We conclude that nifedipine does not differ significantly from placebo in providing relief from acute renal colic.
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PMID:Nifedipine for the relief of renal colic: a double-blind, placebo-controlled clinical trial. 238 74

The effect of nifedipine (Adalat) on isolated dog ureter was compared with that on isolated coronary artery. Nifedipine at a concentration of 10(-8) mol/l significantly decreased the frequency of ureteral rhythmic contractions evoked by potassium, and suppressed the force of these contractions at a concentration of 3 X 10(-8) mol/l. In potassium-contracted coronary artery strips, nifedipine at concentrations more than 3 X 10(-9) mol/l produced significant relaxations in a concentration-dependent manner. The results indicate that nifedipine is able to act inhibitorily on ureteral contractions, and inhibition of pace making activities in ureteral smooth muscle was suggested as a mode of action of nifedipine.
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PMID:Comparison of the effects of nifedipine on ureter and coronary artery isolated from the dog. 403 84

1. Previous studies have established a marked difference in sensitivity to organic calcium channel blockers of the phasic compared with tonic component of the contraction to potassium chloride (KCl) in the guinea-pig ureter. The mechanisms responsible for this difference have remained unsettled. In particular, the possible involvement of non-L-type calcium channels in contractility of the ureter has not been determined. In this study we have re-addressed this problem and, to eliminate any possible contribution of sensory neuropeptides released by KCl from peripheral endings of afferent nerves, all experiments were performed in ureters pre-exposed to the sensory neurone blocking agent, capsaicin (10 microM for 15 min). 2. Increasing concentrations of KCl (10-160 mM) produced phasic and tonic contractions of the guinea-pig isolated ureter: the L-type calcium channel agonist, Bay K 8644 (1 microM), enhanced both components of the contraction to KCl. 3. Nifedipine (1 microM) abolished all responses to increasing concentrations of KCl after 60 min contact time; after a shorter incubation period (15 min), the phasic contractions to low KCl concentrations were still observed, while the tonic responses were abolished. 4. The effects of nifedipine (0.1 nM-1 microM) on the phasic and tonic components of the response to 80 nM KCl were assessed after 15-120 min contact time. Nifedipine was equipotent in inhibiting the tonic response at all times tested, while a marked time-dependency of inhibition toward phasic responses was observed. After 15 min contact time, nifedipine was 181 times more potent in inhibiting tonic than phasic response to KCl, while after 120 min contact time the difference between EC50 values was only 5.4 times. 5. Cadmium chloride (3-30 microM) was equi-effective in inhibiting the phasic and tonic responses to KCl while nickel chloride was ineffective at 10-fold higher concentrations. omega-Conotoxin (0.1 microM) and tetrodotoxin (0.3 microM) were ineffective. 6. The present findings indicate that L-type voltage-dependent calcium channels mediate both phasic and tonic components of the response of the guinea-pig ureter to KCl while neither T-type nor N-type voltage-dependent calcium channels are involved. The marked time-dependency of inhibitory action of nifedipine suggests that L-type voltage-dependent calcium channels which are responsible for the generation of phasic contraction of the ureter are in a low affinity state for interaction with nifedipine.
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PMID:A pharmacological analysis of calcium channels involved in phasic and tonic responses of the guinea-pig ureter to high potassium. 753 37

In supine anesthetized rats, two cannulae were inserted into a unilateral ureter near the kidney and urinary bladder, respectively. Fluid from a reservoir placed approximately 27 cm above the rat was infused into the ureter lumen through the cannula near the kidney, and the resulting peristaltic pressure signals were measured from the cannula near the bladder. When drugs acting on ion channels were applied from the ureter lumen and their effects on the peristaltic pressure signals were studied, the K+ channel opener BRL 38227 (1 x 10(-4) M and 1 x 10(-3) M) was found to decrease the frequency dose-dependently. However, the K+ channel blockers glibenclamide and 4-aminopyridine at 1 x 10(-3) M did not affect peristaltic movement. Nifedipine (1 x 10(-5) M and 1 x 10(-4) M) decreased the frequency of peristalsis, but the effect was weaker than that of BRL 38227. Lidocaine at very high concentration (1.5 x 10(-2) and 1.5 x 10(-1) M) decreased the amplitude and increased the frequency of the peristaltic signals. These results indicate that the K+ channel opener has the most inhibitory effect on ureteral peristaltic function.
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PMID:A simple method for measurement of ureteric peristaltic function in vivo and the effects of drugs acting on ion channels applied from the ureter lumen in anesthetized rats. 769 93

Nifedipine, a calcium channel blocker, was tested for its in vivo effect on the ureter and kidney during acute obstruction. There was no discernible effect on peristalsis but glomerular filtration rate was improved. Thus, nifedipine would not be expected to decrease renal colic from obstruction.
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PMID:Effect of nifedipine on kidney and ureteral function after experimental acute unilateral ureteral obstruction. 848 20

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.
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PMID:Protein kinase A inhibitors selectively inhibit the tonic contraction of the guinea pig ureter to high potassium. 891 54

1. In isolated tissue experiments, neurokinin A (NKA) produced concentration-dependent contraction of human and guinea-pig ureter (pD2 = 6.7 and 7.2, respectively); an effect greatly reduced (>80% inhibition) by the tachykinin NK2 receptor-selective antagonist MEN 11420 (0.1 microM). The tachykinin NK1 and NK3 receptor agonists septide and senktide, respectively, were ineffective. 2. Electrical field stimulation (EFS) of the guinea-pig isolated renal pelvis produced an inotropic response blocked by MEN 11420 (0.01-1 microM). In the same preparation MEN 11420 (0.1 microM) blocked (apparent pK(B) = 8.2) the potentiation of spontaneous motor activity produced by the NK2 receptor-selective agonist [betaAla8]NKA(4-10). 3. In sucrose-gap experiments, EFS evoked action potentials (APs) accompanied by phasic contractions of human and guinea-pig ureter, which were unaffected by tetrodotoxin or MEN 11420 (3 microM), but were blocked by nifedipine (1-10 microM). NKA (1-3 microM) produced a slow membrane depolarization with superimposed APs and a tonic contraction with superimposed phasic contractions. NKA prolonged the duration of EFS-evoked APs and potentiated the accompanying contractions. MEN 11420 completely prevented the responses to NKA in both the human and guinea-pig ureter. 4. Nifedipine (1-10 microM) suppressed the NKA-evoked APs and phasic contractions in both human and guinea-pig ureter, and slightly reduced the membrane depolarization induced by NKA. A tonic-type contraction of the human ureter in response to NKA persisted in the presence of nifedipine. 5. In conclusion, tachykinins produce smooth muscle excitation in both human and guinea-pig ureter by stimulating receptors of the NK2 type only. NK2 receptor activation depolarizes the membrane to trigger the firing of APs from latent pacemakers.
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PMID:Excitatory motor and electrical effects produced by tachykinins in the human and guinea-pig isolated ureter and guinea-pig renal pelvis. 984 36