Omega conotoxin and prejunctional modulation of the biphasic response of the rat isolated urinary bladder to single pulse electrical field stimulation

1991 ◽  
Vol 11 (5) ◽  
pp. 295-304 ◽  
Author(s):  
C. A. Maggi
Keyword(s):  
Urinary Bladder ◽  
Single Pulse ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Biphasic Response ◽  
Electrical Field ◽  
Pulse Electrical Field

Further studies on the motor response of the human isolated urinary bladder to tachykinins, capsaicin and electrical field stimulation

1989 ◽  
Vol 20 (5) ◽  
pp. 663-669 ◽  
Author(s):  
Carlo Alberto Maggi ◽  
Riccardo Patacchini ◽  
Paolo Santicioli ◽  
Damiano Turini ◽  
Gabriele Barbanti ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Motor Response ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field

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.

Effects of Distigmine on Electrical Field Stimulation-Induced Contraction of Mouse Urinary Bladder Smooth Muscles

Pharmacology ◽  
2016 ◽  
Vol 99 (3-4) ◽  
pp. 106-113 ◽  
Author(s):  
Keisuke Obara ◽  
Yurina Kobayashi ◽  
Daisuke Chino ◽  
Yoshio Tanaka
Keyword(s):  
Urinary Bladder ◽  
Smooth Muscles ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field

scholarly journals Nerve-released acetylcholine contracts urinary bladder smooth muscle by inducing action potentials independently of IP3-mediated calcium release

2010 ◽  
Vol 299 (3) ◽  
pp. R878-R888 ◽  
Author(s):  
Bernhard Nausch ◽  
Thomas J. Heppner ◽  
Mark T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Urinary Bladder ◽  
Action Potentials ◽  
Cyclopiazonic Acid ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Bladder Smooth Muscle ◽  
Electrical Field ◽  
Urinary Bladder Smooth Muscle

Nerve-released ACh is the main stimulus for contraction of urinary bladder smooth muscle (UBSM). Here, the mechanisms by which ACh contracts UBSM are explored by determining Ca2+ and electrical signals induced by nerve-released ACh. Photolysis of caged inositol 1,4,5-trisphosphate (IP3) evoked Ca2+ release from the sarcoplasmic reticulum. Electrical field stimulation (20 Hz) induced Ca2+ waves within the smooth muscle that were present only during stimulus application. Ca2+ waves were blocked by inhibition of muscarinic ACh receptors (mAChRs) with atropine and depletion of sarcoplasmic reticulum Ca2+ stores with cyclopiazonic acid (CPA), and therefore likely reflect activation of IP3 receptors (IP3Rs). Electrical field stimulation also increased excitability to induce action potentials (APs) that were accompanied by Ca2+ flashes, reflecting Ca2+ entry through voltage-dependent Ca2+ channels (VDCCs) during the action potential. The evoked Ca2+ flashes and APs occurred as a burst with a lag time of ∼1.5 s after onset of stimulation. They were not inhibited by blocking IP3-mediated Ca2+ waves, but by blockers of mAChRs (atropine) and VDCCs (diltiazem). Nerve-evoked contractions of UBSM strips were greatly reduced by blocking VDCCs, but not by preventing IP3-mediated Ca2+ signaling with cyclopiazonic acid or inhibition of PLC with U73122. These results indicate that ACh released from nerve varicosities induces IP3-mediated Ca2+ waves during stimulation; but contrary to expectations, these signals do not appear to participate in contraction. In addition, our data provide compelling evidence that UBSM contractions evoked by nerve-released ACh depend on increased excitability and the resultant Ca2+ entry through VDCCs during APs.

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