Barrington’s nucleus CRH neurons conditionally drive bladder contraction: A multi-unit optogenetic recording study in mice

2019 ◽  
Vol 18 (1) ◽  
pp. e3-e4
Author(s):  
H. Ito ◽  
A. Sales ◽  
B. Tench ◽  
M.J. Drake ◽  
A.E. Pickering
Keyword(s):  
Bladder Contraction

Synthesis and biological properties of cholecystokinin heptapeptide analogues containing D- and L-forms of tert-leucine or neopentylglycine in position 5

1991 ◽  
Vol 56 (10) ◽  
pp. 2209-2217 ◽  
Author(s):  
Jan Hlaváček ◽  
Jana Pírková ◽  
Jan Pospíšek ◽  
Jiřina Slaninová ◽  
Lenka Maletínská
Keyword(s):  
Gall Bladder ◽  
Solid Phase ◽  
Biological Activities ◽  
Biological Properties ◽  
Phase Synthesis ◽  
Structural Modifications ◽  
Bladder Contraction ◽  
Anorectic Effect ◽  
Carboxy Terminal ◽  
Anorectic Activity

Using solution or solid-phase synthesis we prepared the cholecystokinin fragment Boc-CCK-7 (Boc-Tyr-(SO3-.Na+)-Met-Gly-Trp-Met-Asp-PheNH2) and its four analogues in which the methionine moiety (Met) in the carboxy-terminal part is replaced by tert-leucine (Tle) or neopentylglycine (Neo) residue or D-enantiomers of these non-coded amino acids. These structural modifications led to reduction of the studied biological activities (gall bladder contraction, anorectic activity, analgetic and sedation activity) of all prepared analogues except Boc[Neo5]-CCK-7 which, being less analgetically active, retains full gall bladder and sedation activity of CCK-8. Moreover, its anorectic activity is substantially higher (400%). This analogue is very interesting particularly for its selectively increased (4x) anorectic effect compared with that of CCK-8.

scholarly journals NTPDase1 Modulates Smooth Muscle Contraction in Mice Bladder by Regulating Nucleotide Receptor Activation Distinctly in Male and Female

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 147
Author(s):  
Romuald Brice Babou Kammoe ◽  
Gilles Kauffenstein ◽  
Julie Pelletier ◽  
Bernard Robaye ◽  
Jean Sévigny
Keyword(s):  
Smooth Muscle ◽  
Ex Vivo ◽  
Smooth Muscle Contraction ◽  
Receptor Activation ◽  
Nucleoside Triphosphate ◽  
Nucleotide Receptors ◽  
Nerve Terminals ◽  
Wild Type ◽  
Nucleoside Triphosphate Diphosphohydrolase ◽  
Bladder Contraction

Nucleotides released by smooth muscle cells (SMCs) and by innervating nerve terminals activate specific P2 receptors and modulate bladder contraction. We hypothesized that cell surface enzymes regulate SMC contraction in mice bladder by controlling the concentration of nucleotides. We showed by immunohistochemistry, enzymatic histochemistry, and biochemical activities that nucleoside triphosphate diphosphohydrolase-1 (NTPDase1) and ecto-5′-nucleotidase were the major ectonucleotidases expressed by SMCs in the bladder. RT-qPCR revealed that, among the nucleotide receptors, there was higher expression of P2X1, P2Y1, and P2Y6 receptors. Ex vivo, nucleotides induced a more potent contraction of bladder strips isolated from NTPDase1 deficient (Entpd1−/−) mice compared to wild type controls. The strongest responses were obtained with uridine 5′-triphosphate (UTP) and uridine 5′-diphosphate (UDP), suggesting the involvement of P2Y6 receptors, which was confirmed with P2ry6−/− bladder strips. Interestingly, this response was reduced in female bladders. Our results also suggest the participation of P2X1, P2Y2 and/or P2Y4, and P2Y12 in these contractions. A reduced response to the thromboxane analogue U46619 was also observed in wild type, Entpd1−/−, and P2ry6−/− female bladders showing another difference due to sex. In summary, NTPDase1 modulates the activation of nucleotide receptors in mouse bladder SMCs, and contractions induced by P2Y6 receptor activation were weaker in female bladders.

Induction of urethral closure and inhibition of bladder contraction by continuous magnetic stimulation

1999 ◽  
Vol 18 (5) ◽  
pp. 505-510 ◽  
Author(s):  
Tomonori Yamanishi ◽  
Kosaku Yasuda ◽  
Ryuji Sakakibara ◽  
Shin Suda ◽  
Norio Ishikawa ◽  
...  
Keyword(s):  
Magnetic Stimulation ◽  
Bladder Contraction ◽  
Urethral Closure

Threshold for efferent bladder nerve firing in the rat

1999 ◽  
Vol 276 (6) ◽  
pp. R1819-R1824
Author(s):  
Els van Asselt ◽  
Joost le Feber ◽  
Ron van Mastrigt
Keyword(s):  
Theoretical Model ◽  
Rise Time ◽  
Afferent Nerve ◽  
Bladder Pressure ◽  
Afferent Activity ◽  
Nerve Activity ◽  
Efferent Activity ◽  
Rat Bladder ◽  
Bladder Contraction

In this study, the mechanism involved in the initiation of voiding was investigated. Bladder pressure and bladder and urethral nerve activity were recorded in the anesthetized rat. Bladder nerve activity was resolved into afferent and efferent activity by means of a theoretical model. The beginning of an active bladder contraction was defined as the onset of bladder efferent firing at a certain time ( t 0). From t 0 onward, bladder efferent activity increased linearly during δ t seconds (rise time) to a maximum. The pressure at t 0 was 1.0 ± 0.4 kPa, the afferent nerve activity at t 0 was 2.0 ± 0.6 μV (53 ± 15% of maximum total nerve activity), and δ t was 11 ± 13 s. Between contractions the afferent activity at t 0 was never exceeded. Urethral afferent nerve activity started at bladder pressures of 2.1 ± 1.1 kPa. Therefore, we concluded that urethral afferent nerve activity does not play a role in the initiation of bladder contractions; voiding contractions presumably are initiated by bladder afferent nerve activity exceeding a certain threshold.

Role of endothelin ETA and ETB receptors in the guinea-pig urinary bladder contraction

2003 ◽  
Vol 470 (1-2) ◽  
pp. 99-102 ◽  
Author(s):  
Akira Yoshida ◽  
Yasuko Sakurai-Yamashita ◽  
Kimihiro Yamashita ◽  
Nobuyuki Tanaka ◽  
Kohtaro Taniyama
Keyword(s):  
Urinary Bladder ◽  
Guinea Pig ◽  
Bladder Contraction

Studies on the biphasic nature of urinary bladder contraction and function

1987 ◽  
Vol 6 (4) ◽  
pp. 339-350 ◽  
Author(s):  
Robert M. Levin ◽  
Michael R. Ruggieri ◽  
Harcharan S. Gill ◽  
Niels Haugaard ◽  
Alan J. Wein
Keyword(s):  
Urinary Bladder ◽  
Bladder Contraction ◽  
And Function

scholarly journals Diabetes mellitus- and cooling-induced bladder contraction: an in vitro study

2010 ◽  
Vol 46 (6) ◽  
pp. 321_E3
Author(s):  
Kismet Esra Atalık ◽  
Nilsel Okudan ◽  
Hakki Gokbel ◽  
Serpil Kalkan ◽  
Gokhan Cuce
Keyword(s):  
Diabetes Mellitus ◽  
In Vitro Study ◽  
Vitro Study ◽  
Bladder Contraction

scholarly journals Mechanisms of reflex bladder activation by pudendal afferents

2011 ◽  
Vol 300 (2) ◽  
pp. R398-R407 ◽  
Author(s):  
John P. Woock ◽  
Paul B. Yoo ◽  
Warren M. Grill
Keyword(s):  
Sympathetic Innervation ◽  
Bladder Volume ◽  
Nerve Transection ◽  
Hypogastric Nerve ◽  
Afferent Stimulation ◽  
Adrenergic Antagonist ◽  
Bladder Contraction ◽  
Dorsal Nerve ◽  
Frequency Of Stimulation ◽  
Stimulation Of

Activation of pudendal afferents can evoke bladder contraction or relaxation dependent on the frequency of stimulation, but the mechanisms of reflex bladder excitation evoked by pudendal afferent stimulation are unknown. The objective of this study was to determine the contributions of sympathetic and parasympathetic mechanisms to bladder contractions evoked by stimulation of the dorsal nerve of the penis (DNP) in α-chloralose anesthetized adult male cats. Bladder contractions were evoked by DNP stimulation only above a bladder volume threshold equal to 73 ± 12% of the distension-evoked reflex contraction volume threshold. Bilateral hypogastric nerve transection (to eliminate sympathetic innervation of the bladder) or administration of propranolol (a β-adrenergic antagonist) decreased the stimulation-evoked and distension-evoked volume thresholds by −25% to −39%. Neither hypogastric nerve transection nor propranolol affected contraction magnitude, and robust bladder contractions were still evoked by stimulation at volume thresholds below the distension-evoked volume threshold. As well, inhibition of distention-evoked reflex bladder contractions by 10 Hz stimulation of the DNP was preserved following bilateral hypogastric nerve transection. Administration of phentolamine (an α-adrenergic antagonist) increased stimulation-evoked and distension-evoked volume thresholds by 18%, but again, robust contractions were still evoked by stimulation at volumes below the distension-evoked threshold. These results indicate that sympathetic mechanisms contribute to establishing the volume dependence of reflex contractions but are not critical to the excitatory pudendal to bladder reflex. A strong correlation between the magnitude of stimulation-evoked bladder contractions and bladder volume supports that convergence of pelvic afferents and pudendal afferents is responsible for bladder excitation evoked by pudendal afferents. Further, abolition of stimulation-evoked bladder contractions following administration of hexamethonium bromide confirmed that contractions were generated by pelvic efferent activation via the pelvic ganglion. These findings indicate that pudendal afferent stimulation evokes bladder contractions through convergence with pelvic afferents to increase pelvic efferent activity.

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