Electrophysiological properties of the bladder

Fry, Christopher; Wu, Changhao; Sui, Guiping

doi:10.1007/bf01901509

Cited by 23 publications

(18 citation statements)

References 55 publications

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“…Briefly, the space constant () for decremental current flow measured in detrusor smooth muscle is Ϸ1 mm, compared with a cell length of 150-200 m. Such a 5-to 10-fold difference between the space constant for passive current decay and cell length is a clear indication of the presence of an adequate intercellular pathway (9,(23)(24)(25). Although the resistance of the intercellular pathway in the bladder is clearly much larger than that observed in organs known to be well coupled (e.g., myocardium) (13,23), the membrane resistance of the detrusor myocyte is also correspondingly greater (e.g., than a cardiac myocyte), so that overall, the R m /R i still favors significant intercellular current flow.…”

Section: Discussionmentioning

confidence: 99%

Increased connexin43-mediated intercellular communication in a rat model of bladder overactivity in vivo

Christ

Day²,

Day³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

101

111

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Bladder overactivity associated with outflow obstruction is a common human condition recapitulated in the female rat by narrowing the diameter of the urethra. The goal of these studies was to evaluate the role of intercellular communication through connexin43 (Cx43)-derived gap junction channels to bladder overactivity following partial urethral outflow obstruction of 3-day to 6-wk duration. Cx43 mRNA and protein expression were barely detectable by Northern or Western blots, respectively, in the detrusor layer of normal bladders, but bands were found with both techniques after 6 wk of obstruction. Linear regression analysis of the RT-PCR data revealed a statistically significant positive correlation between the duration of obstruction (again, ranging from 3-day to 6-wk duration) and Cx43 mRNA transcript levels, such that after 6 wk of obstruction, Cx43 transcript levels were ≈15-fold greater than initial control values. When taking into account the approximately fivefold increase in bladder weight over this same time frame, the absolute amount of Cx43 mRNA in the bladder apparently increased by ≈75-fold. In that regard, as anticipated, and consistent with previous observations, 6 wk of obstruction was also associated with a significant increase in spontaneous bladder contractions between micturitions. The amplitude of these contractions was significantly reduced by heptanol given intravesically. Furthermore, carbachol-precontracted bladder strips from obstructed animals were more sensitive to heptanol-induced relaxation (100 μM) than their unobstructed counterparts ( n = 6; P < 0.01). When bladder strips were equivalently precontracted via electrical field stimulation (EFS; 20 Hz), similar heptanol-induced relaxation responses were observed. However, the tetrodotoxin-resistant portion of the EFS-induced contraction was greater in the obstructed than in the unobstructed animals, and this portion of the contractile response was more sensitive to heptanol-induced relaxation in obstructed than unobstructed bladders ( n = 7; P < 0.01). Taken together, these observations indicate that partial outlet obstruction produces an overactive bladder that may be more dependent on intercellular communication through gap junctions for modulation of contractile responses than its normal counterpart.

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Section: Discussionmentioning

confidence: 99%

Increased connexin43-mediated intercellular communication in a rat model of bladder overactivity in vivo

Christ

Day²,

Day³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

101

111

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“…However, the spontaneous contraction of UBSM has been suggested to be intimately associated with action potentials generated in this smooth muscle cell. 1,4,5) Action potentials recorded in UBSM cells are also myogenic in nature, but disappear in the presence of L-type Ca 2ϩ channel inhibitors, showing Ca 2ϩ spike characteristics. Enhancement of Ca 2ϩ entry during a burst of action potentials could induce a phasic contraction in this smooth muscle.…”

mentioning

confidence: 97%

Phospholipase C Inhibitors Suppress Spontaneous Mechanical Activity of Guinea Pig Urinary Bladder Smooth Muscle

Tanaka

Okamoto

Imai

et al. 2003

Biological & Pharmaceutical Bulletin

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Urinary bladder smooth muscle (UBSM) exhibits spontaneous rhythmic contraction. This spontaneous mechanical activity is generated in the presence of neuronal blockade and thus is myogenic in origin. The spontaneous myogenic contraction of UBSM may be the fundamental determinant of the physiological functions of the urinary bladder to store and excrete urine. Although the mechanisms by which UBSM generates spontaneous contraction have not been completely ascertained, its induction has been suggested to be intimately associated with smooth muscle cell action potentials to enhance extracellular Ca(2+) influx through voltage-gated L-type Ca(2+) channels. However, the alteration of membrane electrical activity does not seem to be the exclusive trigger mechanism for the generation of the spontaneous contraction. In the present study, we show that spontaneous mechanical activity of guinea pig UBSM is substantially diminished by an inhibitor of phospholipase C (PLC), U-73122, but is not affected by its inactive form, U-73343. Significant attenuation of the mechanical activity can be also obtained with another PLC inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate. Our present findings suggest a significant role for the activation of PLC and subsequent inositol 1,4,5-trisphosphate-induced Ca(2+) release mechanism as an alternative triggering system for inducing spontaneous mechanical activity of UBSM. The present results support the idea that the action potential is not the sole pacemaker mechanism by which spontaneous contraction is induced in UBSM.

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“…In smooth muscle, the resting membrane potential that is mainly determined by the K ϩ channel activity plays an im- portant role in regulating the contractility through the control of voltage-dependent Ca 2ϩ channel activity (for review, see Kuriyama et al, 1998). However, K ATP channels are unlikely to make a major contribution to the resting membrane potential in the pig detrusor cells, because K ATP channel openings were observed only when the patch pipette contained levcromakalim in the present study (also see review in Fry et al, 1998). Furthermore, K ATP channels in pig detrusor cells are not subject to the neural and hormonal controls, unlike in pancreatic ␤-cells and some vascular smooth muscle cells such as rabbit mesenteric artery, in which K ATP channels are activated by adenosine and several other neuropeptides (Dunne et al, 1989;Nelson et al, 1990;Dart and Standen, 1993;Kleppisch and Nelson, 1995).…”

Section: Discussionmentioning

confidence: 61%

Levcromakalim and MgGDP Activate Small Conductance ATP-Sensitive K⁺ Channels of K⁺ Channel Pore 6.1/Sulfonylurea Receptor 2A in Pig Detrusor Smooth Muscle Cells: Uncoupling of cAMP Signal Pathways

Kajioka

Nakayama

Asano

et al. 2008

J Pharmacol Exp Ther

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Pharmacological studies have suggested the existence of ATPsensitive K ϩ (K ATP ) channel as a therapeutic target in urinary bladders; however, electrical properties have not yet been shown. Patch-clamp techniques were applied to investigate the properties of K ATP channels in pig detrusor cells. In whole-cell configuration, levcromakalim, a K ATP channel opener, induced a long-lasting outward current in a concentration-dependent manner. The current-voltage curve of the levcromakaliminduced membrane current intersected at approximately Ϫ80 mV. This current was abolished by glibenclamide. Intracellular application of 0.1 mM GDP significantly enhanced the levcromakalim-induced membrane current, whereas cAMP did not. Furthermore, neurotransmitters related to cAMP signaling, such as calcitonin gene-related peptide, vasointestinal peptide, adenosine, and somatostatin, had little effect on the membrane current. In cell-attached configuration, levcromakalim activated K ϩ channels with a unitary conductance of ϳ12 pS. When the patch configuration was changed to inside-out mode, the K ϩ channel activity ran down. Subsequent application of 1 mM GDP reactivated the channels. The openings of the ϳ12 pS K ϩ channels in the presence of 1 mM GDP was suppressed by ATP and glibenclamide. In reverse transcription-polymerase chain reaction, K ϩ channel pore 6.1 and sulfonylurea receptor (SUR)2A were predominant in pig detrusor cells. The 12 pS K ϩ channel activated by levcromakalim in pig detrusor smooth muscle cells is a K ATP channel. The predominant expression of SUR2A can account for the lack of effect of neurotransmitters related to cAMP. Kϩ Channels inhibited by intracellular ATP [ATP-sensitive K ϩ (K ATP ) channels] are widely distributed in cells including muscles, neurons, and endocrine cells, allowing the intracellular energy level to be reflected in the membrane potential (Noma, 1983;Cook and Hales, 1984;Spruce et al., 1985;Ashford et al., 1988). In the smooth muscle, the existence of K ATP channels has been shown in single-channel recordings and by use of pharmacological tools, for example, cromakalim and nicorandil (K ATP channel openers) or glibenclamide and tolbutamide (K ATP channel blockers) (Quayle et al., 1997).K ATP channels in smooth muscle cells consist of K ϩ channel pore (Kir)6.1 or -6.2 coupled with sulfonylurea receptors (SUR), forming channels with relatively small conductance (approximately 20 pS) (Isomoto et al., 1996). A well known feature of the smooth muscle K ATP channel is activation by intracellular nucleoside diphosphates (NDP), another index for the intracellular energy level.The functions of the lower urinary tract, such as voiding urine and refilling, are produced by coordinated actions of urinary bladder and urethral smooth muscles. Disharmony of this co-operation is thought to be one of the causes of bladder incontinence (Mostwin, 2002;Brading, 2006). Because pharmacological studies had suggested the existence of K ATP channels in the lower urinary tract smooth muscle, Article, publ...

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Electrophysiological properties of the bladder

Cited by 23 publications

References 55 publications

Increased connexin43-mediated intercellular communication in a rat model of bladder overactivity in vivo

Increased connexin43-mediated intercellular communication in a rat model of bladder overactivity in vivo

Phospholipase C Inhibitors Suppress Spontaneous Mechanical Activity of Guinea Pig Urinary Bladder Smooth Muscle

Levcromakalim and MgGDP Activate Small Conductance ATP-Sensitive K⁺ Channels of K⁺ Channel Pore 6.1/Sulfonylurea Receptor 2A in Pig Detrusor Smooth Muscle Cells: Uncoupling of cAMP Signal Pathways

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Electrophysiological properties of the bladder

Cited by 23 publications

References 55 publications

Increased connexin43-mediated intercellular communication in a rat model of bladder overactivity in vivo

Increased connexin43-mediated intercellular communication in a rat model of bladder overactivity in vivo

Phospholipase C Inhibitors Suppress Spontaneous Mechanical Activity of Guinea Pig Urinary Bladder Smooth Muscle

Levcromakalim and MgGDP Activate Small Conductance ATP-Sensitive K+ Channels of K+ Channel Pore 6.1/Sulfonylurea Receptor 2A in Pig Detrusor Smooth Muscle Cells: Uncoupling of cAMP Signal Pathways

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Levcromakalim and MgGDP Activate Small Conductance ATP-Sensitive K⁺ Channels of K⁺ Channel Pore 6.1/Sulfonylurea Receptor 2A in Pig Detrusor Smooth Muscle Cells: Uncoupling of cAMP Signal Pathways