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Query: UMLS:C0011570 (depression)
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Chlorpromazine (ClP) and trifluoperazine (TFP) depress electrical and mechanical activity of ureter smooth muscle cells. Contraction was depressed by less doses of the substances applied as compared with the processes responsible for generation of spike activity. ClP causes the displacement of the dose-effect curve for Ca2+ towards larger concentrations of the latter. Trifluoperazine displaces the dose-effect curve for contraction to the right and downwards. It is concluded that inhibition of contraction and depression of ClP and TFP spikes is due to the calmodulin blocking on which kinase activity of myosin light chains depends. It is supposed that processes responsible for activation of the membrane systems of Ca2+ transport in the process of spike generation are also calmodulin-dependent.
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PMID:[Study of electromechanical coupling in smooth muscle cells of the ureter using phenothiazines]. 672 4

We have investigated the ability of human alpha CGRP (CGRP) to inhibit the electrically-evoked myogenic contractions of the guinea-pig ureter, in comparison with the K channel opener, cromakalim, and the adenylate cyclase activator, forskolin. CGRP (0.1 nM-0.1 microM) produced a concentration-dependent inhibition of the evoked contractions; its action was prevented by the CGRP receptor antagonist, CGRP(8-37) (1 microM), while it was unaffected by the nitric oxide (NO) synthase inhibitor, L-nitroarginine (30 microM). The effect of CGRP was antagonized in a noncompetitive manner (depression of Emax, no change in EC50) by glibenclamide (1-10 microM), a blocker of ATP-sensitive potassium channels (KATP). A substantial fraction of the inhibitory effect of CGRP was glibenclamide-resistant, however. Glibenclamide also blocked the inhibitory action of cromakalim (0.1-10 microM) without affecting the inhibition produced by forskolin (0.1-30 microM). When tested in a low-K medium (extracellular K reduced from 5.9 to 1.2 mM), the inhibitory effects of CGRP, cromakalim and forskolin were enhanced. The inhibitory effect of forskolin was partly antagonized by glibenclamide when tested in a low-K medium. CGRP (0.1 microM), cromakalim (3 microM) and forskolin (10 microM) inhibited the contractile response to KCl (80 mM), which is characterized by a distinct phasic and tonic component: cromakalim selectively inhibited the phasic response to KCl with CGRP and forskolin inhibited both components. The inhibitory effect of CGRP on the phasic contraction to KCl was partly glibenclamide-(1 microM) sensitive, while that on the tonic contraction was glibenclamide-resistant. The inhibitory action of forskolin on both components of the response to KCl was unchanged by glibenclamide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple mechanisms in the smooth muscle relaxant action of calcitonin gene-related peptide (CGRP) in the guinea-pig ureter. 787 Jan 93

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

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

A 21-year-old male double-yellowheaded Amazon parrot was referred because of possible urolithiasis. The bird had strained to void since it was young, and recently, signs of depression and inappetence had appeared. Radiography revealed 2 mineralized opacities in the left caudal portion of the celomic cavity. A left lateral celiotomy revealed that the left ureter was dilated and contained a calculus, which was later determined to be composed of monosodium uric acid crystals and proteinaceous material. The second mineralized mass could not be located at that time, but was detected in the caudal aspect of the celomic cavity after surgery by use of radiography. Manual attempts to maneuver the uterolith from the ureter through the cloaca were unsuccessful. Five days after the initial surgery, the uterolith was removed by cloacotomy and ventral midline laparotomy. Excretory urography performed 10 and 31 days after surgery revealed that the left ureter was homogeneously opacified and gradually decreased to 3 to 6 mm in diameter. The bird remained healthy and seemed to strain less severely during voiding. Nonspecific signs associated with ureteroliths may result in delay in diagnosis. Surgical removal of ureteroliths may be an effective treatment for this uncommon condition, but it is complicated by certain anatomic features of birds and may result in ureteral stricture.
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PMID:Ureterotomy for removal of two ureteroliths in a parrot. 1099 58

Osmotic pressure maintained by liver or kidney tissue measured by its water equilibrium with solutions of sodium chloride remains unchanged from 5 minutes up to 1(1/2) hours following removal of the tissue from the body. Then with autolytic increase of molecular concentration within the cytoplasm of cells it reaches a higher level. Osmotic pressure maintained by pancreas or submaxillary gland, as ascertained in the same way, remains unchanged during (1/2) hour and later increases. Liver tissue of rat, mouse, guinea pig, rabbit, and cat maintains an osmotic pressure greater than twice that of the blood, and kidney tissue maintains an osmotic pressure somewhat less than twice that of blood. Fasting throughout a period of 7 days has little influence upon osmotic pressure maintained by cells of liver or kidney. Low protein diet has been found to depress osmotic pressure of liver cells after about 4 weeks, and with degenerative changes in the parenchyma, notably fatty infiltration, this pressure has remained at a diminished level during approximately 90 days. Increase of pressure within the common bile duct and the changes following biliary obstruction are accompanied by depression of the osmotic pressure maintained by liver tissue and ligation of the ureter diminishes the osmotic pressure maintained by kidney tissue. In both instances osmotic pressure tends later to rise to its former level. The osmotic pressure maintained by liver or by kidney tissue preserves an approximately uniform level under normal conditions and may be little changed by conspicuous injury to the organ. When this osmotic homeostasis is impaired by severe injury the pressure maintained by the tissue returns to its former level with recovery from the injury.
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PMID:Osmotic homeostasis maintained by mammalian liver, kidney, and other tissues. 1305 14

The most common cause of ureteral obstruction in dogs and cats is ureteral calculi. Common clinical signs associated with ureteral obstruction include abnormalities in urination, persistent urinary tract infection, abdominal pain, vomiting, anorexia, weight loss,and depression or lethargy. Medical management of ureteral obstruction includes fluid diuresis, muscle relaxants, and treatment of azotemia using nephrostomy tubes or hemodialysis. Surgical techniques used to restore patency to the ureter include ureterotomy,partial ureterectomy and ureteroneocystostomy, and ureteral resection and anastomosis. Lithotripsy has been used in dogs to remove ureteral calculi. Renal function can be preserved if complete ureteral obstruction is relieved within several days of onset.
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PMID:Management of ureteral obstruction. 1522 12

Congenital anomalies of the urinary tract in horses may be difficult to diagnose and treat. Presenting complaints are variable and include weight loss, depression, dysuria, hematuria, and mild colic. Although the most severe abnormalities are diagnosed in the neonate, some diseases, such as ectopic ureter(s), may be identified in older horses. In human medicine, the fetus is examined in the prenatal period for evidence of urinary tract dysfunction, but this is not yet common practice in equine medicine. As a result, urinary tract anomalies are diagnosed after birth using a wide variety of diagnostic modalities.
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PMID:Congenital anomalies of the equine urinary tract. 1806 58

A nine-month-old domestic short haired cat was admitted with the history of acute vomiting, depression and shivering. Abdominal ultrasonography revealed minimum enlargement of the right uterine horn filled with anechoic fluid. On excretory urography, functionally and anatomically normal, enlarged left kidney was found, but right kidney was absent. It was preliminary diagnosed as hydrometra with right renal agenesis. Aiming at the correction of hydrometra, we performed ovariohysterectomy. During spaying, we found a missing segment of distal part of the right uterine horn and absence of ipsilateral kidney and ureter. Compressed uterine structure and segmental aplasia of right uterine horn were found in histopathological investigation. Taken together, it was diagnosed as a segmental aplasia of uterine horn with ipsilateral renal agenesis.
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PMID:Segmental aplasia of the uterine horn with ipsilateral renal agenesis in a cat. 1862 11

Previous investigators have found that complete occlusion of the ureter may lead either to hydronephrosis or to atrophy. In Lindemann's series of six dogs;, for instance: Two animals showed simple hydronephrosis, three animals showed simple atrophy, and in one animal the kidney was slightly enlarged and the ureter and pelvis dilated, but fluid was absent. In his series of four rabbits, all showed hydronephrosis. The result, whether hydronephrosis or atrophy, is evidently not determined by the time elapsing after the operation. Lindemann found that the intrapelvic pressure resulting from the ligation obliterates the lumen of the vessels, first of the veins and subsequently of the arteries; but that this is compensated by an increase of the collateral blood supply through the capsule, the degree of this compensation determining the presence or absence of hydronephrosis. If the blood supply is free, the fluid after tapping will accumulate again and again. It is somewhat remarkable that all of our dogs showed hydronephrosis after the first operation. The results of establishing a urinary fistula differed in the two cases in which it was tried: The fluid did not re-form in Dog 3 even when sodium sulphate was injected: whereas in Dog 4, a very abundant quantity of fluid reaccumulated spontaneously; but it differed notably in composition from the original fluid, having more the character of a purulent inflammatory exudate. The histological changes consist in necrosis of the renal cells, obliteration of the glomeruli, increase of connective tissue, and endarteritis and periarteritis. Different areas in the same kidney are affected in very different degree, some areas appearing almost normal. The glomeruli are generally less altered than the tubules. The collecting tubules are generally displaced so as to run parallel to the surface; many are dilated. The changes correspond closely to those described by Lindemann. The sound kidneys showed slight hyperaemia and hypertrophy, but no necrosis. This corresponds with the findings of Pearce and of Ames. The uniformity in chemical composition of the fluid obtained, after the first operation, from the four dogs, as shown by Column III of Table I, is very striking, and points to a uniform origin by a process which is but little affected by the interval elapsing after the operation. The specific gravity, total solids and proteids correspond to those of a very dilute lymph, being but a trifle above those of cerebro-spinal fluid and aqueous humor, and much lower than those of serum, lymph and most cystic fluids (the proteid content of the latter being generally from 2 to 6.5 per cent.). The human fluid (Column II) which had remained in the kidney for a very long time had a particularly low proteid percentage; while that of the second fluid of Dog 4 (Column VIII) was very much higher; this last fluid having a pronounced inflammatory character and being of recent formation. The absence of notable amounts of the specific urinary constituents is particularly important.(4) Odorous principles are entirely absent. Urinary pigments appear to be present in the four dogs' urines, but absent from the human case,(5) and after the second operation in case of the dogs. It seems fair to assume that the pigments were secreted shortly after the ligation, when the kidneys were still functional, and that they were reabsorbed with extreme slowness. Urea was present in all the fluids, but its quantity was very small in the dogs, and probably in the human case. It is on the whole somewhat greater than in the serum (0.103 per cent., in place of 0.05 per cent.), but the difference may be within the analytical error. The same applies to the ammonia, phosphates and sulphates. An important difference between these fluids on the one hand and blood serum, lymph and ordinary exudate on the other, lies in the higher contents of chlorid, and the consequently greater molecular concentration. The ordinary chlorid content of body fluid varies between 0.55 and 0.70 per cent., mean about 0.6 per cent (as NaCl), while that of the first kidney fluid, in the dogs, varied between 0.68 and 0.75 per cent., mean 0.725 per cent.; that of the human fluid was 0.83 per cent., that of the second fluid of Dog 4 only 0.52 per cent. The depression of the freezing point in the human case was 0.715 degrees C., as against the normal value, for human serum, of 0.491 to 0.562. (Possibly the blood of this patient had a higher concentration than normal, since uraemia existed.) The high chlorid percentage has evidently no relation to the length of time during which the fluid sojourned in the kidney. It is probably to be explained by the relatively slow absorption of this ion from the kidney pelvis. It is also to be remarked that cerebrospinal fluids generally have a somewhat high chlorid content (0.573 and 0.6 per cent.), but this never reaches the height of these ureteral fluids.
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PMID:EXPERIMENTAL ATRESIA OF THE URETER. 1986 74


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