scholarly journals Coupled Nitric Oxide and Autonomic Receptor Functional Responses in the Normal and Inflamed Urinary Bladder of the Rat

2012 ◽  
pp. 371-380 ◽  
Author(s):  
R. VESELÁ ◽  
H. ASKLUND ◽  
P. ARONSSON ◽  
M. JOHNSSON ◽  
V. WSOL ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
The Body ◽  
Bladder Function ◽  
Detrusor Muscle ◽  
Functional Responses ◽  
Nitric Oxide Synthase Inhibitor ◽  
Parasympathetic Nerve ◽  
Contractile Responses

Both divisions of the autonomic nervous system are involved in regulation of urinary bladder function. Several substances, other than noradrenaline and acetylcholine, seem to play important roles in physiology and pathophysiology of lower urinary tract. In the current study, we aimed to examine if there exist interplays between nitric oxide (NO) and autonomic transmitters and if such interactions vary in different parts of the urinary bladder in healthy and cyclophosphamide (CYP)-induced cystitic rats; when administered to the animals (100 mg/kg; i.p.), the cytotoxic CYP metabolite acrolein induces bladder inflammation. In the current study a series of in vitro functional studies were performed on detrusor muscle strip preparations. Stimulation with electrical field stimulation (EFS), methacholine, adenosine 5´-triphosphate (ATP), and adrenaline evoked contractile responses in isolated bladder preparations that were significantly reduced in cyclophosphamide (CYP)-treated rats. While the nitric oxide synthase inhibitor Nω nitro-L-arginine (L-NNA; 10-4 M) did not affect contractile responses in normal, healthy strip preparations, it significantly increased the contractile responses to EFS, methacholine and adrenaline, but not to ATP, in the bladders from the CYP-treated rats. In the CYP-treated rats, the ATP-evoked relaxatory part of its dual response (an initial contraction followed by a relaxation) was 6-fold increased in comparison with that of normal preparations, whereas the isoprenaline relaxation was halved in the CYP-treated. While L-NNA (10-4 M) had no effect on the isoprenaline-evoked relaxations, it reduced the ATP-evoked relaxations in strip preparations from the bladder body of CYP-treated rats. Stimulation of β2- and β3 adrenoceptors evoked relaxations and both responses were reduced in cystitis, the latter to a larger extent. In the trigone, the reduced ATP-evoked contractile response in the inflamed strips was increased by L-NNA, while L NNA had no effect on the ATP-evoked relaxations, neither on the relaxations in healthy nor on the larger relaxations in the inflamed trigone. The study shows that both contractile and relaxatory functions are altered in the state of inflammation. The parasympathetic nerve-mediated contractions of the body of the bladder, evoked by the release of ATP and acetylcholine, were substantially reduced in cystitis. The relaxations to β-adrenoceptor and purinoceptor stimulation were also reduced but only the ATP-evoked relaxation involved NO.

A systematic review of mechanisms by which natural products of plant origin evoke vasodilatation

2006 ◽  
Vol 84 (8-9) ◽  
pp. 803-821 ◽  
Author(s):  
J. Robert McNeill ◽  
Tannis M. Jurgens
Keyword(s):  
Nitric Oxide ◽  
Natural Products ◽  
Potassium Channel ◽  
Mechanisms Of Action ◽  
Oxide System ◽  
The Body ◽  
Plant Origin ◽  
Nitric Oxide Synthase Inhibitor ◽  
Channel Function

This article reviews the body of work aimed at elucidating the mechanisms of action by which natural products of plant origin exert a vasodilatory effect at the level of the vasculature. The search was restricted to 4 mechanisms: the nitric oxide system and (or) reactive oxygen species, the eicosanoid system, potassium channel function, and calcium channel function. The National Library of Medicine database was searched using “PubMed” without restriction to language. The search generated 266 references on 15 November 2005. Most studies were in vitro in nature and of these, most involved studies in the rat aorta. Many of the natural products evoked vasodilatation through an endothelium-dependent mechanism. The vasodilatation was attenuated or abolished by a nitric oxide synthase inhibitor and, in some of these studies, by an inhibitor of guanylate cyclase. A few studies reported a cyclooxygenase component, but most found no effect of the cyclooxygenase inhibitor, indomethacin. The vasorelaxation evoked by several natural products was attenuated by various potassium channel blocking agents, suggesting that some natural products exerted their effect either directly or indirectly through activation of potassium channels. Finally, a significant number of natural products evoked vasodilatation either through blockade of calcium channels or by inhibiting the release of calcium from intracellular stores. Many natural products evoked vasodilatation through multiple mechanisms. The information in this review on mechanisms of action should facilitate good clinical practice by increasing the predictive capabilities of the practitioner, notably the ability to predict adverse effects and interactions among medications. The knowledge should also help to provide leads to the ultimate goal of developing new therapeutic medications.

Pharmacologic responses of the mouse urinary bladder

Open Medicine ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. 192-197 ◽  
Author(s):  
A. Canda ◽  
Christopher Chapple ◽  
Russ Chess-Williams
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Detrusor Muscle ◽  
Field Stimulation ◽  
Muscarinic Agonists ◽  
Electrical Field ◽  
M3 Receptor

AbstractThe aim of the study was to determine pathways involved in contraction and relaxation of the mouse urinary bladder. Mouse bladder strips were set up in gassed Krebs-bicarbonate solution and responses to various drugs and electrical field stimulation were obtained. Isoprenaline (b-receptor agonist) caused a 63% inhibition of carbachol precontracted detrusor (EC50=2nM). Carbachol caused contraction (EC50=0.3µM), responses were antagonised more potently by 4-DAMP (M3-antagonist) than methoctramine (M2-antagonist). Electrical field stimulation caused contraction, which was inhibited by atropine (60%) and less by guanethidine and α,β-methylene-ATP. The neurogenic responses were not potentiated by inhibition of nitric oxide synthase. Presence of an intact urothelium significantly depressed responses to carbachol (p=0.02) and addition of indomethacin and L-NNA to remove prostaglandin and nitric oxide production respectively did not prevent the inhibitory effect of the urothelium. In conclusion, b-receptor agonists cause relaxation and muscarinic agonists cause contraction via the M3-receptor. Acetylcholine is the main neurotransmitter causing contraction while nitric oxide has a minor role. The mouse and human urothelium are similar in releasing a factor that inhibits contraction of the detrusor muscle which is unidentified but is not nitric oxide or a prostaglandin. Therefore, the mouse may be used as a model to study the lower urinary tract.

Abstract 18060: TRAIL Promotes Angiogenesis and Ischemia-Induced Neovascularisation via NOX4, H2O2 and Nitric Oxide-Dependent Mechanisms

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Belinda A Di Bartolo ◽  
Sian P Cartland ◽  
Leonel Prado-Lourenco ◽  
Nor Saadah M Azahri ◽  
Thuan Thai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiogenic Factor ◽  
Tubule Formation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Therapeutic Implications ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
First Time

Background: Angiogenesis and neovascularization are essential processes that follow ischemia insults. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) not only induces endothelial cell (EC) death and inhibits angiogenesis, but also promotes EC migration, invasion and proliferation in vitro . These seemingly opposite effects make its role in angiogenesis in vivo unclear. Using TRAIL -/- and wild-type mice, we sought to determine the role of TRAIL in angiogenesis and neovascularisation. We also sought mechanisms in vitro . Methods and Results: Reduced vascularisation assessed by real-time in vivo 3D Vevo ultrasound imaging and CD31 staining was observed in TRAIL -/- mice 28 d after hindlimb ischemia. Moreover, reduced capillary formation and increased apoptosis was evident in TRAIL -/- muscles even at 3 d after ischemic surgery. We have previously shown that fibroblast growth factor-2 (FGF-2), a potent angiogenic factor, regulates TRAIL gene expression in vascular smooth muscle cells. Indeed, FGF-2 also regulates TRAIL expression in ECs, and FGF-2-inducible proliferation, migration and tubule formation was inhibited with siRNA targeting TRAIL. Notably, both FGF-2 and TRAIL significantly increased NOX4 expression. TRAIL-inducible angiogenic activity in ECs was inhibited with siRNAs targeting NOX4, and consistent with these, NOX4 mRNA was reduced in 3 d ischemic hindlimbs of TRAIL -/- mice. TRAIL stimulated intracellular H 2 O 2 levels in ECs, and TRAIL-inducible proliferation, migration and tubule formation was inhibited with not only PEG-catalase, a H 2 O 2 scavenger, but also blocked with L-NAME, a nitric oxide synthase inhibitor. Conclusions: This is the first demonstration showing that TRAIL promotes angiogenesis in vivo . We show for the first time that the TRAIL stimulates NOX4 expression to mediate nitric oxide-dependent angiogenic effects. This has significant therapeutic implications such that TRAIL may improve the angiogenic response to ischemia and increase perfusion recovery in patients with CVD and diabetes.

Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes

2005 ◽  
Vol 288 (6) ◽  
pp. F1220-F1226 ◽  
Author(s):  
Guiming Liu ◽  
Firouz Daneshgari
Keyword(s):  
Urinary Bladder ◽  
Unknown Origin ◽  
Electrical Field Stimulation ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Detrusor Muscle ◽  
Sprague Dawley ◽  
Contractile Responses ◽  
Bladder Detrusor ◽  
Induced Changes

Diabetic bladder dysfunction (DBD) is among the most common and bothersome complications of diabetes mellitus. Autonomic neuropathy has been counted as the cause of DBD. In the present study, we compared the alterations in the neurogenically mediated contractile responses of urinary bladder in rats with streptozocin-induced diabetes, 5% sucrose-induced diuresis, and age-matched controls. Male Sprague-Dawley rats were divided into three groups: 9-wk diabetic rats, diuretic rats, and age-matched controls. Micturition and morphometric characteristics were evaluated using metabolic cage and gross examination of the bladder. Bladder detrusor muscle strips were exposed to either periodic electrical field stimulation (EFS) or to EFS in the presence of atropine, α,β-methylene adrenasine 5′-triphosphate, or tetrodotoxin. The proportions of cholinergic, purinergic, and residual nonadrenergic-noncholinergic (NANC) components of contractile response were compared among the three groups of animals. Diabetes caused a significant reduction of body weight compared with diuresis and controls, although the bladders of diabetic and diuretic rats weighed more than the controls. Both diabetes and diuresis caused significant increase in fluid intake, urine output, and bladder size. Diabetes and diuresis caused similarly increased response to EFS and reduced response to cholinergic component compared with controls. However, the purinergic response was significantly smaller in diuretic bladder strips compared with controls but not in diabetic rats. A residual NANC of unknown origin increased significantly but differently in diabetics and diuretics compared with controls. In conclusion, neurogenically mediated bladder contraction is altered in the diabetic rat. Diabetic-related changes do not parallel diuretic-induced changes, indicating that the pathogenesis of DBD needs further exploration.

scholarly journals Injectable Gel Form of a Decellularized Bladder Induces Adipose-Derived Stem Cell Differentiation into Smooth Muscle Cells In Vitro

2020 ◽  
Vol 21 (22) ◽  
pp. 8608
Author(s):  
Victoria Moreno-Manzano ◽  
Daria Zaytseva-Zotova ◽  
Eric López-Mocholí ◽  
Álvaro Briz-Redón ◽  
Berit Løkensgard Strand ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Smooth Muscle Cells ◽  
Stem Cell Differentiation ◽  
Muscle Cells ◽  
Enzymatic Digestion ◽  
Biological Properties ◽  
Detrusor Muscle ◽  
Extracellular Matrix Components

Biologic scaffolds composed of extracellular matrix components have been proposed to repair and reconstruct a variety of tissues in clinical and pre-clinical studies. Injectable gels can fill and conform any three-dimensional shape and can be delivered to sites of interest by minimally invasive techniques. In this study, a biological gel was produced from a decellularized porcine urinary bladder by enzymatic digestion with pepsin. The enzymatic digestion was confirmed by visual inspection after dissolution in phosphate-buffered saline solution and Fourier-transform infrared spectroscopy. The rheological and biological properties of the gel were characterized and compared to those of the MatrigelTM chosen as a reference material. The storage modulus G’ reached 19.4 ± 3.7 Pa for the 30 mg/mL digested decellularized bladder gels after ca. 3 h at 37 °C. The results show that the gel formed of the porcine urinary bladder favored the spontaneous differentiation of human and rabbit adipose-derived stem cells in vitro into smooth muscle cells to the detriment of cell proliferation. The results support the potential of the developed injectable gel for tissue engineering applications to reconstruct for instance the detrusor muscle part of the human urinary bladder.

Viral respiratory infection increases alveolar macrophage cytoplasmic motility in rats: role of NO

1995 ◽  
Vol 268 (3) ◽  
pp. L399-L406 ◽  
Author(s):  
T. Fukushima ◽  
K. Sekizawa ◽  
M. Yamaya ◽  
S. Okinaga ◽  
M. Satoh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Viral Infection ◽  
Respiratory Infection ◽  
Sendai Virus ◽  
The Body ◽  
Particle Rotation ◽  
Nitrite Production ◽  
Viral Respiratory Infection ◽  
Viral Respiratory

Ingested ferrimagnetic (Fe3O4) particles were used to estimate noninvasively the motion of organelles in alveolar macrophages (AM) in intact rats during viral respiratory infection by parainfluenza type 1 (Sendai) virus. Four days after instillation of Fe3O4 particles (3 mg/kg) into the lung, remnant field strength (RFS) was measured at the body surface immediately after magnetization of Fe3O4 particles by an externally applied magnetic field. RFS decreases with time, due to particle rotation (relaxation) which is related to cytoplasmic motility of AM. Viral infection increased the relaxation rate (lambda o per min), and increases in lambda o reached a maximum 3 days after nasal inoculation (day 3). Viral infection (day 3)-induced increases in lambda o were dose dependently inhibited by either the L-arginine analogue N-nitro-L-arginine or by methylene blue, an inhibitor of guanylate cyclase activity. Bronchoalveolar lavage fluid obtained from infected rats contained significantly higher levels of nitrite than that from control rats (P < 0.01). In in vitro experiments, AM from infected rats showed significantly higher lambda o, nitrite production, and intracellular guanosine 3',5'-cyclic monophosphate levels than those from control rats (P < 0.01). Sodium nitroprusside, known to release nitric oxide concentration dependently, increased lambda o of AM from noninfected rats in vitro. These results suggest that nitric oxide plays an important role in AM cytoplasmic motility during viral respiratory infection.

Simulation of In Vitro-Like Electrical Activities in Urinary Bladder Smooth Muscle Cells

2017 ◽  
Vol 33 ◽  
pp. 45-51
Author(s):  
Chitaranjan Mahapatra ◽  
Rohit Manchanda
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Neurotransmitter Release ◽  
Compartment Model ◽  
Bladder Smooth Muscle ◽  
Parasympathetic Nerve ◽  
Stochastic Nature ◽  
Urinary Bladder Smooth Muscle ◽  
Electrical Activities

Urinary bladder smooth muscle (UBSM) generates spontaneous electrical activities due to stochastic nature of purinergic neurotransmitter release from the parasympathetic nerve. The stochastic nature of the purinergic neurotransmitter release was represented by a simplified ‘point-conductance’ model to mimic in vitro-like electrical activities in UBSM cell. The point-conductance was represented by the independent synaptic conductance described by the stochastic random-walk processes and injected into a single-compartment model of mouse UBSM cell. This model successfully evoked irregular spontaneous depolarizations (SDs) and spontaneous action potential (sAP) as the properties of in vitro-like electrical activities in UBSM cells. The model mimics the T- and L-type Ca2+ ion channel blocker by setting their respective conductance to zero. We also found that the point-conductance model modulates the sAP properties by adding background activity.

Involvement of β3-adrenoceptors in mouse urinary bladder function: Role in detrusor muscle relaxation and micturition reflex

2009 ◽  
Vol 618 (1-3) ◽  
pp. 76-83 ◽  
Author(s):  
Aurore Deba ◽  
Stefano Palea ◽  
Celine Rouget ◽  
Timothy D Westfall ◽  
Philippe Lluel
Keyword(s):  
Urinary Bladder ◽  
Muscle Relaxation ◽  
Bladder Function ◽  
Detrusor Muscle ◽  
Micturition Reflex

Role of Nitric Oxide in Urinary Bladder Function: Effect of L-Arginine

2007 ◽  
Vol 78 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Catherine Whitbeck ◽  
Paul Chichester ◽  
Rebekah Sokol ◽  
Robert M. Levin
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Bladder Function
Sign in / Sign up

Export Citation Format

Share Document