Molecular basis of voltage-dependent delayed rectifier K+ channels in smooth muscle cells from rat tail artery

Xu, Chuanli; Tang, Guanghua; Lu, Yanjie; Wang, Rui

doi:10.1016/s0024-3205(00)00529-4

Cited by 27 publications

(13 citation statements)

References 23 publications

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“…3) Relative to Kv2.1, protein levels of Kv1.2 and Kv1.5 may be low, thus limiting our ability to detect a significant decrease in expression. In support of the latter, the kinetics and voltage dependences of activation and steady-state inactivation of I Kv reported here resemble those of heterologously expressed Kv2.1 channels (37) or native currents attributed to Kv2.1 channels (25). Furthermore, the reduction of I Kv was proportionally similar to the reduction of Kv2.1 protein (Ϸ50% for each).…”

Section: Nfatc3 Controls Smooth Muscle Excitabilitysupporting

confidence: 78%

“…Note, however, that a recent study concluded that Kv1.2 and Kv1.5 make a substantial contribution to I Kv in middle cerebral arteries (24). Regardless, Kv2.1 has been shown to be expressed and hyperpolarize vascular smooth muscle from mesenteric (38), tail (25), aortic (39), and pulmonary (40) arteries. Thus, activation of CaN and NFAT may modulate the excitability of numerous arterial beds by regulating Kv2.1 expression.…”

Section: Nfatc3 Controls Smooth Muscle Excitabilitymentioning

confidence: 98%

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NFATc3 Regulates Kv2.1 Expression in Arterial Smooth Muscle

Amberg

Rossow

Navedo

et al. 2004

Journal of Biological Chemistry

127

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Voltage-gated K؉ (Kv) channels control the excitability of arterial smooth muscle. However, the molecular mechanisms regulating Kv channel function in smooth muscle remain unclear. We examined the hypothesis that the vasoactive peptide angiotensin II (Ang II) regulates arterial smooth muscle Kv channel function via calcineurin-dependent activation of the transcription factor NFAT. We found that sustained administration of Ang II decreased Kv currents (I Kv ) by reducing the expression of Kv2.1 K ؉ channel subunits. This effect of Ang II was independent of pressure but required Ca 2؉ influx through L-type Ca 2؉ channels. Consistent with our hypothesis, we found that calcineurin and NFATc3 are obligatory components of the signaling cascade mediating reduced I Kv by Ang II. We conclude that sustained Ang II exposure increases smooth muscle Ca 2؉ , which leads to activation of calcineurin and NFATc3, culminating in decreased Kv2.1 expression and reduced I Kv function. These results support the novel concept that NFATc3 controls the excitability of arterial smooth muscle by regulating Kv2.1 expression.

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Section: Nfatc3 Controls Smooth Muscle Excitabilitysupporting

confidence: 78%

Section: Nfatc3 Controls Smooth Muscle Excitabilitymentioning

confidence: 98%

NFATc3 Regulates Kv2.1 Expression in Arterial Smooth Muscle

Amberg

Rossow

Navedo

et al. 2004

Journal of Biological Chemistry

127

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“…While the exact function of the current in smooth muscles has yet to be clarified, it most likely plays a role in the regulation of cellular excitability. Kv4.1-3 primary subunits as well as ␤-subunits have been detected in rat mesenteric, tail, and pulmonary arteries (218,219). Indeed, a long splice variant (with a 19-amino acid insert compared with brain) of Kv4.3 was first cloned from rat vas deferens and is found in rat aortic smooth muscle as well as other smooth muscles (145).…”

Section: For a Review) A-type Kmentioning

confidence: 99%

Structure and Function of Kv4-Family Transient Potassium Channels

Birnbaum

Varga

et al. 2004

Physiological Reviews

328

360

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Shal-type (Kv4.x) K+ channels are expressed in a variety of tissue, with particularly high levels in the brain and heart. These channels are the primary subunits that contribute to transient, voltage-dependent K+ currents in the nervous system (A currents) and the heart (transient outward current). Recent studies have revealed an enormous degree of complexity in the regulation of these channels. In this review, we describe the surprisingly large number of ancillary subunits and scaffolding proteins that can interact with the primary subunits, resulting in alterations in channel trafficking and kinetic properties. Furthermore, we discuss posttranslational modification of Kv4.x channel function with an emphasis on the role of kinase modulation of these channels in regulating membrane properties. This concept is especially intriguing as Kv4.2 channels may integrate a variety of intracellular signaling cascades into a coordinated output that dynamically modulates membrane excitability. Finally, the pathophysiology that may arise from dysregulation of these channels is also reviewed.

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“…Transcripts of a variety of pore-forming ␣-subunits with A-type properties (i.e., Kv1.4, Kv3.3, Kv3.4, Kv4.1, Kv4.2, and Kv4.3) have been detected in rat mesenteric and tail arteries (122,123). Kv ␤-subunits, which confer A-type properties to some delayed rectifier pore-forming subunits (e.g., Ref.…”

mentioning

confidence: 99%

A-type potassium currents in smooth muscle

Amberg

Koh

Imaizumi

et al. 2003

American Journal of Physiology-Cell Physiology

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A-type currents are voltage-gated, calcium-independent potassium (Kv) currents that undergo rapid activation and inactivation. Commonly associated with neuronal and cardiac cell-types, A-type currents have also been identified and characterized in vascular, genitourinary, and gastrointestinal smooth muscle cells. This review examines the molecular identity, biophysical properties, pharmacology, regulation, and physiological function of smooth muscle A-type currents. In general, this review is intended to facilitate the comparison of A-type currents present in different smooth muscles by providing a comprehensive report of the literature to date. This approach should also aid in the identification of areas of research requiring further attention.

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Molecular basis of voltage-dependent delayed rectifier K+ channels in smooth muscle cells from rat tail artery

Cited by 27 publications

References 23 publications

NFATc3 Regulates Kv2.1 Expression in Arterial Smooth Muscle

NFATc3 Regulates Kv2.1 Expression in Arterial Smooth Muscle

Structure and Function of Kv4-Family Transient Potassium Channels

A-type potassium currents in smooth muscle

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