Changes in Calcium-Dependent Potassium Conductance of Isolated Smooth Muscle Cells of the Rat Bladder in Experimental Diabetes

Kryshtal, D. A.; Paduraru, Oksana M.; Boldyriev, Oleksiy I.; Kit, Oleg; Rekalov, Volodymyr V.; Shuba, Yaroslav

doi:10.1615/intjphyspathophys.v3.i1.80

Cited by 2 publications

(4 citation statements)

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“…However, unlike the previous study (102), the authors found that the mRNA expression for the BK channel ␣-subunit increased, whereas the expression of the BK channel ␤1-subunit decreased in diabetes (74). The authors concluded that these changes in BK channel expression and function enhance UBSM excitability leading to DO/OAB (74). A third study that also uses streptozotocininduced diabetic rats, reported differential effects of BK channel modulators in isolated UBSM strips from control and diabetic rats, suggesting altered BK channel function and/or expression that may contribute to diabetic cystopathy in this rat model (147).…”

Section: Role Of Bk Channels In Ubsm Pathophysiologycontrasting

confidence: 90%

“…The authors speculated that the differences in UBSM responses to iberiotoxin may be due to changes in the channel biophysical properties or intracellular Ca 2ϩ concentrations, as no changes in BK channel expression levels have been observed in diabetic UBSM (102). A more recent study, which uses patch-clamp electrophysiology, reported reduction of the depolarization-induced steady-state BK current density, as well as the TBKC frequency and amplitude in UBSM cells isolated from streptozotocin-induced diabetic rats compared with control rats (74). However, unlike the previous study (102), the authors found that the mRNA expression for the BK channel ␣-subunit increased, whereas the expression of the BK channel ␤1-subunit decreased in diabetes (74).…”

Section: Role Of Bk Channels In Ubsm Pathophysiologymentioning

confidence: 99%

“…A more recent study, which uses patch-clamp electrophysiology, reported reduction of the depolarization-induced steady-state BK current density, as well as the TBKC frequency and amplitude in UBSM cells isolated from streptozotocin-induced diabetic rats compared with control rats (74). However, unlike the previous study (102), the authors found that the mRNA expression for the BK channel ␣-subunit increased, whereas the expression of the BK channel ␤1-subunit decreased in diabetes (74). The authors concluded that these changes in BK channel expression and function enhance UBSM excitability leading to DO/OAB (74).…”

Section: Role Of Bk Channels In Ubsm Pathophysiologymentioning

confidence: 99%

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Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology

Petkov

2014

American Journal of Physiology-Regulatory, Integrative and Comp

133

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The physiological functions of the urinary bladder are to store and periodically expel urine. These tasks are facilitated by the contraction and relaxation of the urinary bladder smooth muscle (UBSM), also known as detrusor smooth muscle, which comprises the bladder wall. The large-conductance voltage- and Ca(2+)-activated K(+) (BK, BKCa, MaxiK, Slo1, or KCa1.1) channel is highly expressed in UBSM and is arguably the most important physiologically relevant K(+) channel that regulates UBSM function. Its significance arises from the fact that the BK channel is the only K(+) channel that is activated by increases in both voltage and intracellular Ca(2+). The BK channels control UBSM excitability and contractility by maintaining the resting membrane potential and shaping the repolarization phase of the spontaneous action potentials that determine UBSM spontaneous rhythmic contractility. In UBSM, these channels have complex regulatory mechanisms involving integrated intracellular Ca(2+) signals, protein kinases, phosphodiesterases, and close functional interactions with muscarinic and β-adrenergic receptors. BK channel dysfunction is implicated in some forms of bladder pathologies, such as detrusor overactivity, and related overactive bladder. This review article summarizes the current state of knowledge of the functional role of UBSM BK channels under normal and pathophysiological conditions and provides new insight toward the BK channels as targets for pharmacological or genetic control of UBSM function. Modulation of UBSM BK channels can occur by directly or indirectly targeting their regulatory mechanisms, which has the potential to provide novel therapeutic approaches for bladder dysfunction, such as overactive bladder and detrusor underactivity.

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Section: Role Of Bk Channels In Ubsm Pathophysiologycontrasting

confidence: 90%

Section: Role Of Bk Channels In Ubsm Pathophysiologymentioning

confidence: 99%

Section: Role Of Bk Channels In Ubsm Pathophysiologymentioning

confidence: 99%

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Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology

Petkov

2014

American Journal of Physiology-Regulatory, Integrative and Comp

133

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“…The impaired functions of BK channels in hypertensive and diabetic vascular SMCs may primarily result from the downregulated b1 subunits. [79][80][81][82] It has been reported that diabetes causes a decrease in BK channel activity and b1 subunit mRNA expression in diabetic UBSMCs, 83 suggesting that the diabetic downregulation of BK channels may promote UBSMC excitability leading to OAB. In support of this finding, a previous study has shown that diabetic mice exhibit decreased voiding efficiency and other OAB characteristics.…”

Section: Role Of Ryanodine Receptors In Bk Channelmediated Physiologimentioning

confidence: 99%

Big-conductance Ca²⁺-activated K⁺ channels in physiological and pathophysiological urinary bladder smooth muscle cells

et al. 2016

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Contraction and relaxation of urinary bladder smooth muscle cells (UBSMCs) represent the important physiological functions of the bladder. Contractile responses in UBSMCs are regulated by a number of ion channels including big-conductance Ca- activated K (BK) channels. Great progress has been made in studies of BK channels in UBSMCs. The intent of this review is to summarize recent exciting findings with respect to the functional interactions of BK channels with muscarinic receptors, ryanodine receptors (RyRs) and inositol triphosphate receptors (IPRs) as well as their functional importance under normal and pathophysiological conditions. BK channels are highly expressed in UBSMCs. Activation of muscarinic M receptors inhibits the BK channel activity, facilitates opening of voltage-dependent Ca (Ca) channels, and thereby enhances excitability and contractility of UBSMCs. Signaling molecules and regulatory mechanisms involving RyRs and IPRs have a significant effect on functions of BK channels and thereby regulate cellular responses in UBSMCs under normal and pathophysiological conditions including overactive bladders. Moreover, BK channels may represent a novel target for the treatment of bladder dysfunctions.

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Changes in Calcium-Dependent Potassium Conductance of Isolated Smooth Muscle Cells of the Rat Bladder in Experimental Diabetes

Cited by 2 publications

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Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology

Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology

Big-conductance Ca²⁺-activated K⁺ channels in physiological and pathophysiological urinary bladder smooth muscle cells

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Changes in Calcium-Dependent Potassium Conductance of Isolated Smooth Muscle Cells of the Rat Bladder in Experimental Diabetes

Cited by 2 publications

References 0 publications

Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology

Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology

Big-conductance Ca2+-activated K+ channels in physiological and pathophysiological urinary bladder smooth muscle cells

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Big-conductance Ca²⁺-activated K⁺ channels in physiological and pathophysiological urinary bladder smooth muscle cells