Response Of Urinary Bladder Research Articles

Dopamine Receptor Subtypes That Induce Hyperactive Urinary Bladder Response in Anesthetized Rats

In anesthetized rats, SKF 38393 (10 mg/kg, i.v.) did not facilitate urinary bladder motility, but bromocriptine (BR, 5 mg/kg, i.v.) alone and the combination of BR (1 mg/kg, i.v.) and SKF 38393 (1 mg/kg, i.v.) induced a hyperactive bladder response (HBR). Both HBR induced by BR alone or BR and SKF 38393 combined was suppressed by SCH 23390, sulpiride or haloperidol. These results indicate that HBR is mediated by the activation of D-2 receptors, and the effects of D-2 agonists on bladder motility are potentiated by the simultaneous stimulation of D-1 receptors.

Sequential Morphological Changes in the Pig Detrusor in Response to Chronic Partial Urethral Obstruction

The sequential morphological changes which occur in the wall of the porcine urinary bladder in response to experimentally induced partial outflow obstruction have been determined using morphometric light and electron microscope techniques. The initial morphological response to urethral obstruction was a reduction of approximately 50% in the density of autonomic nerves in the bladder wall which occurred within the first 3 months. During this period the morphology of smooth muscle cells and the distribution of connective tissue were unaltered. Longer periods of obstruction produced a gradual further reduction in the density of innervation. However, from 3 months onwards the detrusor muscle bundles became infiltrated by connective tissue, although significant change in muscle cell size was not detected after obstruction for 12 months. Using electron microscopy, smooth muscle cells were observed to possess extensive amounts of perinuclear granular reticulum, this feature being particularly marked in bladders subjected to longer periods of obstruction. The underlying mechanisms responsible for these structural changes remain to be determined.

Pharmacological Responses of Rabbit Urinary Bladder after Subtotal Cystectomy

Partial cystectomy is used clinically in specific circumstances. There have been some reports indicating that the bladder following subtotal cystectomy can regenerate to a certain degree. The present study investigates the physiology and pharmacology of bladder regeneration at eight weeks after resection of a major part of the bladder body in rabbits. The following studies were performed on control and cystectomy bladders: 1) in vivo cystometry (prior to and four weeks after the operation, and before the sacrifice at eight weeks); 2) sequential muscle strip study (the strips were obtained by dividing bladder transversely into upper body, lower body, mid-bladder, upper base and lower base); and 3) in vitro whole bladder studies. The results can be summarized as follows: 1) grossly there was no regeneration of the bladder body; the cystometric capacity was increased slowly after the operation primarily due to increased size and capacity of the bladder base. 2) The contractile response of the subtotal cystectomized bladder body to field stimulation and bethanechol stimulation was less than the response of normal bladder body. 3) The contractile response to epinephrine showed that the ratio of alpha/beta adrenergic response was much greater in the cystectomy bladder than in the normal bladder. 4) In the whole bladder study, the intravesical pressure response to field stimulation was about the same in both groups, the response to bethanechol was less for cystectomized bladder, and the response to methoxamine was greater for the cystectomized bladder. 5) The ability of cystectomy bladder to empty in response to both field stimulation and bethanechol was impaired whereas the control bladder fully emptied to both field stimulation and bethanechol.In conclusion, over the eight week period following subtotal cystectomy the capacity increased via distention (and hypertrophy) of the bladder base area as opposed to regeneration of the bladder body. (J. Urol., 142: 409-412, 1989)

Water flow in the toad urinary bladder in response to vasopressin: role of potassium

In agreement with previous reports, we found that absence of K+ from the serosal bath of the toad urinary bladder substantially impairs vasopressin and cAMP-stimulated water flow. The decreased response to vasopressin appears unrelated to prostaglandin production since inhibition of endogenous prostaglandins by pretreatment with naproxen 10(-5) M failed to prevent the effect seen with K+-free Ringer's. The resistance to vasopressin does not appear to be directly related to epithelial K+ concentrations, in that maneuvers leading to decreased intracellular K+ failed to produce a similar effect. A more likely explanation appears to be that K+-free Ringer's induces an increased cytosolic Ca++ which, in turn, decreases the hydrosmotic effects of vasopressin. Several lines of evidence argue in favor of such an explanation: (a) Increased cytosolic Ca++ had been found in other tissues with low extracellular K+; (b) The resistance to vasopressin decreases with decreased serosal Ca++; (c) The effects of K+-free Ringer's are not additive in situations believed to have increased epithelial Ca++, i.e. replacement of serosal Na+ with choline; (d) The effects of K+-free serosal bathing medium could be both prevented and/or reversed if already established by increasing serosal bath, and presumably intracellular, pH, which is believed to decrease intracellular Ca++.

Water flow in the toad urinary bladder in response to vasopressin: role of potassium

In agreement with previous reports, we found that absence of K+ from the serosal bath of the toad urinary bladder substantially impairs vasopressin and cAMP-stimulated water flow. The decreased response to vasopressin appears unrelated to prostaglandin production since inhibition of endogenous prostaglandins by pretreatment with naproxen 10−5 M failed to prevent the effect seen with K+-free Ringer's. The resistance to vasopressin does not appear to be directly related to epithelial K+ concentrations, in that maneuvers leading to decreased intracellular K+ failed to produce a similar effect. A more likely explanation appears to be that K+-free Ringer's induces an increased cytosolic Ca++ which, in turn, decreases the hydrosmotic effects of vasopressin. Several lines of evidence argue in favor of such an explanation: (a) Increased cytosolic Ca++ had been found in other tissues with low extracellular K+; (b) The resistance to vasopressin decreases with decreased serosal Ca++; (c) The effects of K+-free Ringer's are not additive in situations believed to have increased epithelial Ca++, i.e. replacement of serosal Na+ with choline; (d) The effects of K+-free serosal bathing medium could be both prevented and/or reversed if already established by increasing serosal bath, and presumably intracellular, pH, which is believed to decrease intracellular Ca++.

P-305 - The study of hyperactive urinary bladder response induced by apomorphine in anesthetized rats

P-305 - The study of hyperactive urinary bladder response induced by apomorphine in anesthetized rats

Electrical transients produced by the toad urinary bladder in response to altered medium osmolality.

1. The effects of changes in media osmolality on the transepithelial current through the toad urinary bladder under voltage-clamp conditions have been studied. Over the limited range (+/- 24 mosmol/kg H2O) used in these investigations, changes in the osmolality of the mucosal bathing fluid produced no changes in transepithelial current. 2. Changes in osmolality of the serosal fluid greatly affected the transepithelial current with a decrease (increase) in osmolality producing a sustained increase (decrease) in current. 3. The changes in steady-state current were approximately proportional to the magnitude of the osmotic steps and were reproducible and reversible if the osmolalities of the solutions were confined to a domain of 220-260 mosmol/kg H2O. 4. Amiloride, which was used to block all active current, also eliminated the electrical responses to an osmotic pulse, indicating that the responses were of cellular origin. 5. The effects of substituting gluconate for medium chloride were examined. Similar responses were observed, indicating that they were not due to changes in a plasma membrane chloride conductance. 6. The transient currents observed during the changes from one steady state to the other often contained an oscillatory component, the amplitude and the degree of damping of which varied between bladders. The amplitude of the oscillations, but not their frequency, could be varied by altering the magnitude of the osmotic pulse and by changing the imposed transepithelial voltage. Decreasing the electrical potential of the mucosal solution with respect to that of the serosal solution decreased the amplitude of the oscillations, as did increased serosal potassium or substitution of gluconate for serosal chloride. The period of the oscillations always remained within the range of 9-12 min. 7. The results suggest that two major processes are initiated by an osmotic step in the serosal bathing medium. The first involves the establishment of new ion gradients and the second, alterations in sodium pump activity. In addition, there is evidence for a voltage-dependent sodium conductance in the apical membrane.

Bladder Vasodilatation and Release of Vasoactive Intestinal Polypeptide from the Urinary Bladder of the Cat in Response to Pelvic Nerve Stimulation

In the feline urinary bladder blood flow was determined by means of a direct blood flow measurement technique before and during pelvic nerve stimulation. Simultaneous sampling of venous blood from the bladder was performed, and the output of vasoactive intestinal polypeptide (VIP) was determined by means of radioimmunoassay.Maximal stimulation of the pelvic nerves led to a clearcut increase in intravesical pressure and a small but sustained increase of blood flow in the bladder wall. These changes were associated with a drastic increase in VIP output from the bladder, increasing from a control level of 0.2fmol./min. to 15fmol./min. during stimulation.The results suggest that VIP might be the neurotransmitter responsible for the vasodilatation in the feline urinary bladder in response to pelvic nerve stimulation. The discrepancy between the moderate blood flow increase and the pronounced increase in VIP-release might, however, indicate that VIP exerts its main effects elsewhere in the bladder than in the vascular bed, for instance the detrusor smooth muscle. (J. Urol., 138: 671–673, 1987)

Electron microscopic cytochemical localization of Ca-ATPase in toad urinary bladder.

The calcium-regulating enzyme calcium adenosine triphosphatase (Ca-ATPase) was localized in the epithelium of amphibian urinary bladder by the one-step electron microscopic cytochemical procedure. The enzyme was identified along the basolateral border of the epithelial cells that comprise the bladder mucosa. The electron-dense precipitate indicating Ca-ATPase activity was seen in association with the outer leaflet of the basolateral plasmalemmae. Intracellularly, Ca-ATPase activity was seen in association with the mitochondrial matrix of the mitochondria-rich cells. Ca-ATPase was not seen along the apical microvillated border. Enzyme activity was also not seen after incubation in substrate-free media, calcium-free media, or incubation in the presence of vanadate. However, Ca-ATPase activity was evident when the calcium in the standard reaction medium was deleted in favor of magnesium. Addition of antidiuretic hormone (ADH; vasopressin) increased both the basolateral Ca-ATPase reaction and the mitochondrial reaction. Such data appear to indicate further that changes in cytosolic calcium ion concentration take place during the response of amphibian urinary bladder to the polypeptide hormone vasopressin.

Antidiuretic hormone response in the amphibian urinary bladder: Time course of cytochalasin-induced vacuole formation, an ultrastructural study employing ruthenium red

Cytochalasin is known to inhibit the antidiuretic hormone-induced hydro-osmotic response (bulk water flow) in the amphibian urinary bladder without altering hormone-stimulated diffusional water permeability or short-circuit current. In addition, histological studies have shown that the mold metabolite induces the formation of large intracellular vacuoles or lakes in the epithelial cells. We report here a transmission electron microscopic time-course study which indicates that during the early phases of the ADH response cytochalasin causes the formation of numerous multivesicular bodies or aggregates derived from individual basolateral pinocytotic vesicles. Because of their apparent hypertonic nature, the vesicles, as well as the vesicular aggregates, accumulate water during hormone-stimulated hydro-osmotic flow. As a result, the multivesicular bodies dilate and fuse to form the large intracellular lakes characteristic of cytochalasin treatment in the presence of both an applied osmotic gradient and vasopressin. In the presence of mucosal ruthenium red, the luminal glycocalyx was heavily stained with this tracer. At no time, however, even in the presence of hormone, was there any evidence for the uptake of this dye at the apical epithelial border. In the presence of serosal ruthenium red, the lateral intercellular spaces, basolateral pinocytotic vesicles, basal lamina, and collagen, as well as other subepithelial structures, were ruthenium positive. With cytochalasin D, vasopressin, and serosal ruthenium red, both the pinocytotic vesicles and the multivesicular bodies demonstrated an apparent membrane associated ruthenium positive coat. The tracer data indicates that the basolateral pinocytotic vesicles, increased by the presence of hormone, are indeed endocytotic in nature. The mucopolysaccharide coat associated with these structures may be involved in ionic and/or fluid transport.

Changes in Vascular Resistance in the Feline Urinary Bladder in Response to Bladder Filling

The effect of bladder filling on vesical blood flow was studied in anesthetized cats. The pelvic nerves were sectioned and the bladder venous outflow was recorded by a drop counter. Filling of the bladder induced a sustained increase in vesical blood flow, related to the bladder volume. Thus, injection of 10, 20 and 30ml. of saline decreased bladder vascular resistance by 27, 47 and 52 per cent, respectively. This vasodilatation occurred despite a steady state increase in bladder pressure by 25 to 50cm. H2O. Upon emptying of the bladder, blood flow decreased towards control values. The response was unaffected by α-adrenoceptor blockade (phentolamine), β-adrenoceptor blockade (propranolol) and muscarinic cholinoceptor blockade (atropine). The vasodilatation was eliminated by papaverine, indicating that the response was not due to a rearrangement of the vessels at large bladder volumes. The vasodilatation was not associated with any increase in the concentrations of vasoactive intestinal polypeptide (VIP) or substance P in the venous effluent blood. Indomethacin significantly reduced the vasodilatation induced by filling. We conclude that local mechanisms, possibly involving release of prostaglandins, are involved in the vasodilatation following bladder distension.

Streptozocin-induced diabetes affects rat urinary bladder response to autonomic agents

Streptozocin-induced diabetes affects rat urinary bladder response to autonomic agents

Streptozocin-induced diabetes affects rat urinary bladder response to autonomic agents.

The response of the urinary bladder body and base to autonomic agents was studied in streptozocin (STZ)-diabetic rats. The bladder body region from 6-wk diabetic rats showed no changes in response to acetylcholine, phenylephrine, or isoproterenol. In contrast, the bladder base region showed a 39% increase in contractile response to acetylcholine and a 37% increased response to phenylephrine. In tissues from 47-wk diabetic animals, the bladder body showed a 51% increased contractile response to acetylcholine and a 37% increased relaxation response to isoproterenol. The bladder base showed a 66% increased contraction to acetylcholine. Thus, in the bladder base, enhanced responses to acetylcholine are detected soon after induction of diabetes and continue to increase as the diabetic state progresses. Moreover, in the same bladder region, an increase in responsiveness to alpha-adrenergic stimuli occurs. In the bladder body, enhanced responses to cholinergic and to beta-adrenergic stimuli occur, but are only observed in a more chronic diabetic state. The data suggest that an effect associated with autonomic diabetic neuropathy of the urinary bladder is an increased postsynaptic responsiveness to cholinergic stimuli in both regions.

EFFECTS OF AMINOGLYCOSIDE ANTIBIOTICS ON THE CONTRACTILE RESPONSE OF GUINEA-PIG URINARY BLADDER

EFFECTS OF AMINOGLYCOSIDE ANTIBIOTICS ON THE CONTRACTILE RESPONSE OF GUINEA-PIG URINARY BLADDER

EFFECTS OF CEPHALOSPORIN ANTIBIOTICS ON THE CONTRACTILE RESPONSE OF GUINEA-PIG URINARY BLADDER

The present study was undertaken to investigate the effects of cephalothin(CET), cephalexin(CEX),and 7-aminocephalosporanic acid(7-ACA)on the contractile response of guinea-pig urinary bladder. CET,CEX,and 7-ACA in the concentration of 1x10-4g/m1-1x10-4g/m1 had no effect on the transmural electrical stimulation-induced contractile responses.These agents in the concentration of 1x10-8g/m1 slightly reduced them as 97•}3%(n=12),97

Ca2+- and H+-dependent effects of crude bacterial phospholipase C on the hydroosmotic response of toad urinary bladder to serosal hypertonicity.

Phospholipase C (EC 3.1.4.3.) from Clostridium perfringens (crude extracts) was used to study the role of phospholipids in the osmotic permeability of the urinary bladder of the toad. When added to the serosal bath (430 mU/ml) it inhibited the effects of antidiurectic hormone (ADH) and exogenous cyclic AMP. Under the same conditions the increase in osmotic flow produced by serosal hypertonicity (SH) was slightly enhanced by the lipase. The hydroosmotic effect of SH was greatly potentiated by the lipase by decreasing 10-fold the Ca2+ concentration. The SH-induced flow was inhibited by the lipase if the Ca2+ or the H+ concentration was increased 10-fold, but not if the increase in positive charges was produced by a concentration of Mg2+. Phospholipase C had no effect on the action of either ADH or SH if added to the mucosal bath. Serosal neuraminidase or phospholipase A2 could not mimic the effect of phospholipase C on SH. The effect of phospholipase C on the response to SH was not modified if fatty acid-free bovine serum albumin was added to the bath. Therefore, the release of products of lipolysis into the bath do not seem to be responsible for the effects of phospholipase C on SH-induced water flow. The results suggest that the effects of the enzyme on the composition and rearrangement of lipids at the basolateral membrane produce modifications of the water flow. Ca2+ and H+ may modify the enzyme-substrate interaction, suggesting that different phospholipids may be differentially involved in the control of water permeability of the basolateral membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of aminobenzyl penicillin (AB-PC), methylchlorophenyl isoxazolyl penicillin (MCI-PC) and 6-aminopenicillanic acid (6-APA) on the contractile response of guinea-pig urinary bladder.

The present study was undertaken to investigate the effects of aminobenzyl penicillin (AB-PC), methylchlorophenyl isoxazolyl penicillin (MCI-PC), and 6-aminopenicillanic acid (6-APA) on the contractile response of guinea-pig urinary bladder. AB-PC, MCI-PC, and 6-APA, respectively, diminished the intramural electrical stimulation-induced contractile response. AB-PC had almost no effect on the contractile response to exogenous acetylcholine, while MCI-PC remarkably reduced it. The reducing effect of MCI-PC was greater on the intramural electrical stimulation-induced contractile response than it is on the exogenous acetylcholine-induced contractile response. 6-APA slightly reduced the exogenous acetylcholine-induced contractile response. The reducing effect of 6-APA was a little weaker on the exogenous acetylcholine-induced contractile response than it is on the intramural electrical stimulation-induced contractile response. By the addition of AB-PC, the amplitude of spontaneous contractile response of the tissue was reduced gradually with light lowering of the tonus level of the tissue was almost prevented with a little lowering of the tonus level of the tissue. The effects of AB-PC and MCI-PC on the spontaneous contractile response of the tissue mentioned above were also observed in the presence of tetrodotoxin. On the other hand, by the addition of 6-APA, the reducing effect on the amplitude of spontaneous contractile response of the tissue and increasing effect on its frequency were recognized with remarkable raise of the tonus level of the tissue. These phenomena which were induced by 6-APA were also observed in the presence of tetrodotoxin. From these results, the conclusion comes as follows: 1) AB-PC may affect not only on the muscle but also on the intramural cholinergic nerves. 2) MCI-PC may affect on the muscle, but its effect on the intramural nerves is also not likely to be negligible at this time. 3) 6-APA may affect mainly on the muscle.

Structural and functional response of toad urinary bladder to LiCl

AbstractStructural and functional response of toad urinary bladder to LiCl. The physiological and morphological response of toad urinary bladder was examined during mucosal exposure of LiCl both with and without vasopressin (VP). With 20 or 100 mU/ml of VP in the serosal bath there was a decrease in Jv between the first and second VP stimulation in LiCl-treated bladders (VP20, -14 ± 6%; VP100, -16 ± 5%) that was not different from that observed without LiCl (VP20, -8 ± 3%, P = NS). However, with 1 mU/ml of VP, a significant decrease in Jv was evident in LiCl-treated (-30 ± 10%) versus control sacs (+6 ± 8%; P < 0.02). At all VP concentrations tested, a significant decrease in SCC and PD was observed between the first stimulation without LiCl and the second stimulation with LiCl. Both osmotic (Pf) and diffusional water permeability (Pd) were increased significantly with 11 mM LiCl only, while neither basal nor VP-stimulated urea permeability (Pu) was affected. Morphological changes paralleled the physiological alterations induced by LiCl. These data demonstrate that LiCl interferes with the osmotic response of the toad bladder to low concentrations of VP, and increases both Pf and Pd while leaving Pu unaffected. These findings coupled with the cell swelling and intracellular vacuolization suggest the presence of a defect in transepithelial water movement somewhere beyond the apical membrane of the granular cell exposed to LiCl.Réponse structurelle et fonctionnelle de la vessie de crapaud au LiCl. La réponse physiologique et morphologique de la vessie de crapaud a été examinée pendant exposition de la muqueuse à du LiCl en présence ou en l'absence de vasopressine (VP). Pour 20 ou 100 mU/ml de VP dans le bain séreux, il y avait une diminution de Jv entre la première et la seconde stimulation par VP dans les vessies traitées par le LiCl (VP20, -14 ± 6%; VP100, -16 ± 5%), qui n'étaient pas différentes de celles observées sans LiCl (VP20, -8 ± 3%; P = NS). Cependant, avec 1 mU/ml de VP, une diminution significative de Jv était évidente dans les sacs traités au LiCl (-30 ± 10%) par rapport aux sacs contrôles (+6 ± 8%; P < 0,02). Pour toutes les concentrations de VP testées, une diminution significative du SCC et de PD a été observée entre la première stimulation sans LiCl, et la seconde stimulation avec LiCl. Les perméabilités osmotiques (Pf) et diffusionnelles (Pd) à l'eau étaient augmentées significativement avec 11 mM de LiCl seulement tandis que la perméabilité à l'urée basale ou stimulée par la VP (Pu) n'était pas affectée. Des modifications morphologiques allaient de pair avec les altérations physiologiques induites par le LiCl. Ces données démontrent que LiCl interfère avec la réponse osmotique de la vessie de crapaud pour de faibles concentrations de VP, augmente Pf et Pd, mais laisse Pu inchangé. Ces résultats, couplés avec le gonflement cellulaire et la vacuolisation intracellulaire suggèrent la présence d'un défaut du mouvement transépithélial d'eau quelque part au delà de la membrane apicale de la cellule granulaire exposée au LiCl.

Electrical and mechanical activity recorded from rabbit urinary bladder in response to nerve stimulation.

Responses of the smooth muscle membrane of the rabbit bladder to intramuscular nerve stimulation were investigated by the micro-electrode and double sucrose-gap methods. The cell generated regular spontaneous action potentials. Acetylcholine produced a maintained increase in the frequency and ATP a transient increase. Noradrenaline only increased the frequency at very high concentrations. Application of short current pulses (50 microseconds) produced an initial excitatory junction potential (e.j.p.) with a superimposed spike, followed by a late depolarization. On some occasions, hyperpolarization of the membrane appeared between initial e.j.p. and the late depolarization. All these responses were abolished by tetrodotoxin. The late depolarization was enhanced by pre-treatment with neostigmine and abolished by atropine. This means that the delayed depolarization is due to activation of the muscarinic receptor. When the late depolarization was abolished, the amplitude of hyperpolarization was enhanced. The e.j.p. and contraction were unaffected by guanethidine, phentolamine, methysergide, mepyramine, quinidine or theophylline. This means that the e.j.p. is not mediated by activation of adrenergic, tryptaminergic, histaminergic or purinergic receptors. ATP reduced the amplitude of the e.j.p. due to depolarization of the membrane and reduction in the membrane resistance. The amplitude of the e.j.p. was gradually reduced by repetitive stimulation (0.5-2.0 Hz). However, the rate of depression was unchanged in the presence of ATP. Dipyridamole did not change the electrical and mechanical responses to field stimulation. These results do not support the proposal that ATP is the non-cholinergic excitatory transmitter. Apamine and tetraethylammonium (TEA) suppressed the hyperpolarization produced by field stimulation but guanethidine did not inhibit the hyperpolarization. Therefore, the hyperpolarization is due to increased K conductance of the membrane but it is not possible to conclude whether this component is due to the inhibitory action of a neurotransmitter or solely to after hyperpolarization of the spike. It was concluded that the rabbit bladder receives both cholinergic and noncholinergic excitatory neurones.

Role of calcium and prostaglandins in the antidiuretic hormone response: Effect of ionophore A23187

The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E 2 (PGE 2). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.