IP3 decreases coronary artery tone via activating the BKCa channel of coronary artery smooth muscle cells in pigs

Yang, Yan; Li, Pengyun; Cheng, Jun; Cai, Fang; Lei, Ming; Tan, Xiaoqiu; Li, Miaoling; Liu, Zhi-Fei; Zeng, Xiaorong

doi:10.1016/j.bbrc.2013.08.079

Cited by 15 publications

(18 citation statements)

References 17 publications

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“…IP 3 binds to IP 3 receptor (IP 3 R), which facilitates Ca 2ϩ release from the SR, raising intracellular Ca 2ϩ concentration in the form of Ca 2ϩ transients (105) that are believed to trigger UBSM contractions (7,95,145,159). Recent reports suggest that BK channels may be functionally linked and regulated by the IP 3 /IP 3 Rs in some smooth muscle cells, including urethral smooth muscle (76,157,160). It is unknown, however, whether IP 3 or Ca 2ϩ release from the IP 3 Rs activates the BK channels in UBSM to regulate cell excitability and contractility.…”

Section: Ubsm Bk Channel Regulation By Ca 2ϩ Signalsmentioning

confidence: 99%

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: Ubsm Bk Channel Regulation By Ca 2ϩ Signalsmentioning

confidence: 99%

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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“…Arteriolar vasoconstriction induced by elevated PO 2 in hamster cremaster muscle is enhanced by TEA, suggesting that BK Ca channels are activated during this process (672). In porcine coronary arteries, IP 3 has been proposed to directly activate BK Ca channels, contributing to the negative-feedback regulation of vasoconstrictor-induced SMC tone (1582). Thus, vasoconstriction appears to be associated with an increase in BK Ca channel activity, rather than a decrease as predicted from the studies mentioned above.…”

Section: Bkca Channelsmentioning

confidence: 99%

“…10). IP 3 R-related modulation of BK Ca channels also has been proposed to contribute to the negative feedback regulation of tone in porcine coronary arteries (1582). …”

Section: Inositol-145-triphosphate Receptorsmentioning

confidence: 99%

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Tykocki

Boerman

Jackson

2017

Comprehensive Physiology

270

347

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Vascular tone of resistance arteries and arterioles determines peripheral vascular resistance, contributing to the regulation of blood pressure and blood flow to, and within the body’s tissues and organs. Ion channels in the plasma membrane and endoplasmic reticulum of vascular smooth muscle cells (SMCs) in these blood vessels importantly contribute to the regulation of intracellular Ca2+ concentration, the primary determinant of SMC contractile activity and vascular tone. Ion channels provide the main source of activator Ca2+ that determines vascular tone, and strongly contribute to setting and regulating membrane potential, which, in turn, regulates the open-state-probability of voltage gated Ca2+ channels (VGCCs), the primary source of Ca2+ in resistance artery and arteriolar SMCs. Ion channel function is also modulated by vasoconstrictors and vasodilators, contributing to all aspects of the regulation of vascular tone. This review will focus on the physiology of VGCCs, voltage-gated K+ (KV) channels, large-conductance Ca2+-activated K+ (BKCa) channels, strong-inward-rectifier K+ (KIR) channels, ATP-sensitive K+ (KATP) channels, ryanodine receptors (RyRs), inositol 1,4,5-trisphosphate receptors (IP3Rs), and a variety of transient receptor potential (TRP) channels that contribute to pressure-induced myogenic tone in resistance arteries and arterioles, the modulation of the function of these ion channels by vasoconstrictors and vasodilators, their role in the functional regulation of tissue blood flow and their dysfunction in diseases such as hypertension, obesity, and diabetes.

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“…91 It has been reported that activation of IP 3 Rs causes the opening of BK channels in coronary artery SMCs and consequently decreases the artery tone. 92 Whether such a functional interaction between IP 3 Rs and BK channels exists in UBSMCs is not known. As in vascular SMCs, activation of IP 3 Rs may increase or decrease the excitability and contractility of UBSMCs by modulating BK channel activity.…”

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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IP3 decreases coronary artery tone via activating the BKCa channel of coronary artery smooth muscle cells in pigs

Cited by 15 publications

References 17 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

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

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

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IP3 decreases coronary artery tone via activating the BKCa channel of coronary artery smooth muscle cells in pigs

Cited by 15 publications

References 17 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

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

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