Action of angiotensin II, 5‐hydroxytryptamine and adenosine triphosphate on ionic currents in single ear artery cells of the rabbit

Hughes, Alun D.; Bolton, T. B.

doi:10.1111/j.1476-5381.1995.tb16424.x

Cited by 21 publications

(14 citation statements)

References 56 publications

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“…The very small amplitude of single channel currents activated by TG and BAPTA in mouse and rabbit aortic SMC might explain why these channels have not been described previously. Indeed, many different types of nonselective cation channels have been described in SMC (15,(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37), but the single channel properties and mechanism of activation of the 3-pS channel distinguish it from all of the channels found in SMC so far (for review, see Refs. 5, 38, and 39).…”

Section: Store-operated Channel In Smooth Muscle 7786mentioning

confidence: 99%

Properties of a Native Cation Channel Activated by Ca2+ Store Depletion in Vascular Smooth Muscle Cells

Trepakova

Gericke

Hirakawa

et al. 2001

Journal of Biological Chemistry

135

127

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Depletion of intracellular Ca2؉ stores activates capacitative Ca 2؉ influx in smooth muscle cells, but the native storeoperated channels that mediate such influx remain unidentified. Recently we demonstrated that calcium influx factor produced by yeast and human platelets with depleted Ca 2؉ stores activates small conductance cation channels in excised membrane patches from vascular smooth muscle cells (SMC). Here we characterize these channels in intact cells and present evidence that they belong to the class of storeoperated channels, which are activated upon passive depletion of Ca 2؉ stores. Application of thapsigargin (TG), an inhibitor of sarco-endoplasmic reticulum Ca 2؉ ATPase, to individual SMC activated single 3-pS cation channels in cell-attached membrane patches. Channels remained active when inside-out membrane patches were excised from the cells. Excision of membrane patches from resting SMC did not by itself activate the channels. Load-ing SMC with BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid), which slowly depletes Ca 2؉ stores without a rise in intracellular Ca (4, 8) and certain members of the diverse family of TRP channels (9, 10) are thought to be responsible for CCE. However, to date the existence of neither of those has been established in SMC. Importantly, depletion of Ca 2ϩ stores was shown to trigger not only Ca 2ϩ , but also Na ϩ influx in arterial myocytes (11), which implies that store-operated channels in SMC are poorly selective for cations. In freshly isolated mouse anococcygeus SMC there are strong indications that CCE results from activation of a whole cell nonselective cation current (12, 13), although in rat aortic SMC line A7r5 no currents were detected which could be associated with CCE (14, 15). It is totally unclear if the same or different storeoperated channels mediate CCE in SMC from different preparations.Here for the first time we characterize 3-pS cation channels that are activated by Ca 2ϩ store depletion in intact SMC from mouse and rabbit aorta. These channels, contrary to highly Ca 2ϩ -selective CRAC channels, are poorly selective for monoand divalent cations, and under physiological conditions they will allow both Ca 2ϩ and Na ϩ to enter SMC. Recently we found that these channels can also be activated in excised membrane patches by calcium influx factor (CIF) partially purified from human platelets or yeast with depleted Ca 2ϩ stores (16). Taken together, these data strongly support the idea that the native 3-pS channels, which we found in SMC, belong to the class of store-operated ion channels. Preliminary data have been reported in abstract form (17, 18). EXPERIMENTAL PROCEDURES SMC PreparationFour different preparations of aortic SMC were used in our experiments, and the 3-pS channel described in this paper was found to be the same in acutely dispersed and cultured SMC from mouse and rabbit aorta. Most of the experiments on characterization of the single channels and whole cell currents were done on mSMC in short term culture because they pr...

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Section: Store-operated Channel In Smooth Muscle 7786mentioning

confidence: 99%

Properties of a Native Cation Channel Activated by Ca2+ Store Depletion in Vascular Smooth Muscle Cells

Trepakova

Gericke

Hirakawa

et al. 2001

Journal of Biological Chemistry

135

127

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“…Enhanced Ca 2+ influx occurs via direct activation of Ca 2+ -permeable channels as well as indirect voltage-dependent elevation of Ca 2+ channel activity through membrane depolarization [2][3][4]. Ang II has been shown to depolarize vascular smooth muscle via the activation of non-selective inward cation currents [5], or the suppression of outward currents mediated by large conductance Ca 2+ -activated K + channels [6,7], voltage-dependent K + channels [8,9] or ATPsensitive K + (K ATP ) channels [10,11].…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II-activated protein kinase C targets caveolae to inhibit aortic ATP-sensitive potassium channels

Sampson

Davies

Barrett‐Jolley

et al. 2007

Cardiovascular Research

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Objective: The vasoconstrictor angiotensin II (Ang II) acts at G q/11 -coupled receptors to suppress ATP-sensitive potassium (K ATP ) channel activity via activation of protein kinase C (PKC). The aim of this study was to determine the PKC isoforms involved in the Ang II-induced inhibition of aortic K ATP channel activity and to investigate potential mechanisms by which these isoforms specifically target these ion channels.Methods and results: We show that the inhibitory effect of Ang II on pinacidil-evoked whole-cell rat aortic K ATP currents persists in the presence of Gö6976, an inhibitor of the conventional PKC isoforms, but is abolished by intracellular dialysis of a selective PKCε translocation inhibitor peptide. This suggests that PKC-dependent inhibition of aortic K ATP channels by Ang II arises exclusively from the activation and translocation of PKCε. Using discontinuous sucrose density gradients and Western blot analysis, we show that Ang II induces the translocation of PKCε to cholesterol-enriched rat aortic smooth muscle membrane fractions containing both caveolin, a protein found exclusively in caveolae, and Kir6.1, the pore-forming subunit of the vascular K ATP channel. Immunogold electron microscopy of rat aortic smooth muscle plasma membrane sheets confirms both the presence of Kir6.1 in morphologically identifiable regions of the membrane rich in caveolin and Ang II-evoked migration of PKCε to these membrane compartments. Conclusions: Ang II induces the recruitment of the novel PKC isoform, PKCε, to arterial smooth muscle caveolae. This translocation allows PKCε access to K ATP channels compartmentalized within these specialized membrane microdomains and highlights a potential role for caveolae in targeting PKC isozymes to an ion channel effector.

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“…Angiotensin II (Ang II) modulates various types of ion channels. For example, Ang II activates a nonselective cation channel 12 and Ca 2ϩ channels in vascular smooth muscle cells. 13,14 Ang II also inhibits the voltage-dependent K ϩ (Kv) channel and ATP-sensitive K ϩ (K ATP ) channel by activating Ca 2ϩ -independent PKC in vascular smooth muscle cells [15][16][17][18] and inhibits the Ca 2ϩ -activated K ϩ (BK Ca ) channel independently of PKC in vascular smooth muscle cells.…”

mentioning

confidence: 99%

Increased Inhibition of Inward Rectifier K ⁺ Channels by Angiotensin II in Small-Diameter Coronary Artery of Isoproterenol-Induced Hypertrophied Model

Park

Kim

et al. 2007

ATVB

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Objective-We investigated the effects of angiotensin II (Ang II) on inward rectifier K ϩ (Kir) channels in small-diameter coronary arterial smooth muscle cells (SCASMCs) of control and isoproterenol (Iso)-induced hypertrophied rabbits. Methods and Results-Kir current amplitude and Kir channel protein expression were definitely lower in the Iso-induced hypertrophied model than in the control. In a pressurized arterial experiment, 15 mmol/L K ϩ -induced vasodilation was greater in the control arteries than in the arteries of Iso-induced hypertrophied model. Ang II reduced the Kir current in a concentration-dependent manner, and this inhibition was greater in SCASMCs from Iso-induced hypertrophied model than from control. Although, there was no difference in the expression of Ang II type 2 (AT 2 ) receptor between SCASMCs of control and Iso-induced hypertrophied model, the expression of Ang II type 1 (AT 1 ) receptor and phosphorylated PKC␣ were greater in SCASMCs of Iso-induced hypertrophied model than of control. Conclusion-Ang II inhibits Kir channels more prominently in SCASMCs of Iso-induced hypertrophied model owing to increases in the expression of AT 1 receptor and the activation of PKC␣. Our findings about the differential expression of Kir channels and different modulation of Kir channels by a vasoconstrictor (Ang II) in a hypertrophy model are important for better understanding the responsiveness of small-diameter arteries during hypertrophy. (Arterioscler

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Action of angiotensin II, 5‐hydroxytryptamine and adenosine triphosphate on ionic currents in single ear artery cells of the rabbit

Abstract: 4 These data suggest that angiotensin II, 5-HT and ATP activate similar cationic conductances which are relatively non-selective allowing mono-and divalent cations to cross the smooth muscle cell membrane. These channels may allow the influx of calcium under physiological conditions.

Cited by 21 publications

References 56 publications

Properties of a Native Cation Channel Activated by Ca2+ Store Depletion in Vascular Smooth Muscle Cells

Properties of a Native Cation Channel Activated by Ca2+ Store Depletion in Vascular Smooth Muscle Cells

Angiotensin II-activated protein kinase C targets caveolae to inhibit aortic ATP-sensitive potassium channels

Increased Inhibition of Inward Rectifier K ⁺ Channels by Angiotensin II in Small-Diameter Coronary Artery of Isoproterenol-Induced Hypertrophied Model

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Action of angiotensin II, 5‐hydroxytryptamine and adenosine triphosphate on ionic currents in single ear artery cells of the rabbit

Abstract: 4 These data suggest that angiotensin II, 5-HT and ATP activate similar cationic conductances which are relatively non-selective allowing mono-and divalent cations to cross the smooth muscle cell membrane. These channels may allow the influx of calcium under physiological conditions.

Cited by 21 publications

References 56 publications

Properties of a Native Cation Channel Activated by Ca2+ Store Depletion in Vascular Smooth Muscle Cells

Properties of a Native Cation Channel Activated by Ca2+ Store Depletion in Vascular Smooth Muscle Cells

Angiotensin II-activated protein kinase C targets caveolae to inhibit aortic ATP-sensitive potassium channels

Increased Inhibition of Inward Rectifier K + Channels by Angiotensin II in Small-Diameter Coronary Artery of Isoproterenol-Induced Hypertrophied Model

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Increased Inhibition of Inward Rectifier K ⁺ Channels by Angiotensin II in Small-Diameter Coronary Artery of Isoproterenol-Induced Hypertrophied Model