Modulation of calcium‐activated non‐selective cation channel activity by nitric oxide in rat brown adipose tissue.

Koivisto, Ari; Nedergaard, Jan

doi:10.1113/jphysiol.1995.sp020790

Cited by 32 publications

(20 citation statements)

References 25 publications

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“…In agreement with our earlier observations [8][9][10][11], channel activity was spontaneously induced when the patches were excised into extracellular solution or when perfused by intracellular solution (fig. 1A).…”

Section: Resultssupporting

confidence: 80%

Regulation of the Activity of 27 pS Nonselective Cation Channels in Excised Membrane Patches from Rat Brown-Fat Cells

Koivisto

Klinge²,

Nedergaard³

et al. 1998

Cell Physiol Biochem

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The regulation of the activity of the ≈30 pS nonselective cation channel (NSC channel) was studied by the patch-clamp technique in inside-out patches obtained from rat brown-fat cells. NSC channel activity was induced by excision; reduced redox state induced by dithiothreitol accelerated the kinetics in the excised state. The NSC channels were inhibited by the fenamates flufenamic acid and mefenamic acid but not by NS-1619 or SKF-96365. The channels were inhibited by purine nucleotides but not by polyamines. No evidence for protein kinase C, CaM kinase or protein kinase A activation of the NSC channel was obtained. NSC-channel activity was stimulated in a concentration-dependent manner by Ca²⁺ but the EC₅₀ was very high (0.81 mM), in comparison to expected cytosolic Ca²⁺ levels. In the presence of ATP, even higher Ca²⁺ levels were necessary for comparable NSC-channel activation. The increase in P_o was not associated with an increase in open-time constants. We conclude that although high Ca²⁺ levels can experimentally activate the NSC channel, a further mediatory step must probably be postulated in order to link α₁-adrenergic stimulation to NSC-channel activation.

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Section: Resultssupporting

confidence: 80%

Regulation of the Activity of 27 pS Nonselective Cation Channels in Excised Membrane Patches from Rat Brown-Fat Cells

Koivisto

Klinge²,

Nedergaard³

et al. 1998

Cell Physiol Biochem

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“…NO can also modulate sensory information [12], as also shown by our previous study in which NO synthesis in the rat inferior colliculus was found to influence the transmission of acoustic signals to the auditory cortex [11]. Moreover, NO has been described to affect ion channel activity, including Ca 2+ -activated K + channels in colon muscle cells [33], non-selective cation channels in rat brown adipose tissue [16], Na + channels in arterial baroreceptors [19] and Ntype Ca 2+ channels in sympathetic neurons [4].…”

Section: Introductionmentioning

confidence: 60%

Ca 2+ channel inhibition induced by nitric oxide in rat insulinoma RINm5F cells

Grassi¹,

D’Ascenzo²,

Valente³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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The effect of nitric oxide (NO) donors on high-voltage-activated Ca2+ channels in insulin-secreting RINm5F cells was investigated using the patch-clamp technique in the whole-cell configuration. Sodium nitroprusside (SNP, 2-400 microM) induced a dose-dependent reduction in Ba2+ currents with maximal inhibition of 58%. The IC50 for SNP was 45 microM. A different NO donor, (+/-)S-nitroso-N-acetylpenicillamine (SNAP, 500 microM), also produced a 50% decrease in current amplitude. When 200 microM SNP was administered together with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidozoline-1-oxyl-3-oxide (carboxy-PTIO, 300 microM), the Ba2+ current inhibition was lowered to 7%. Administration of 500 microM 8-bromoguanosine 3':5'-cyclic monophosphate sodium salt (8-Br-cGMP) mimicked the effects of SNP, causing a comparable decrease (56%) in peak-current amplitude. When soluble guanylyl cyclase was blocked by 10 microM 1H-[1,2, 4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ), the inhibitory effect of 200 microM SNP was reduced from 39% to 15%. The SNP-induced current decrease was 36% of controls after the blockade of L-type Ca2+ channels and 30% in the presence of 2.5 microM omega-conotoxin-MVIIC. These data indicate that NO inhibits both L-type and P/Q-type Ca2+ channels in RINm5F cells, probably by an increase in the intracellular levels of cGMP. NO may then significantly influence the Ca2+-dependent release of hormones from secretory cells as well as that of neurotransmitters from nerve terminals.

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“…The SV channel shares many similarities with channels belonging to the category of cation-selective calcium-activated channels. In animal cells, several calcium-activated non-selective cation channels of the plasma- (Koivisto and Nedergaard 1995;Eguiguren et al 1996;Saitow et al 1997) and organelle-membranes [e.g. the channel of the sarcoplasmic reticulum (Coronado et al 1994;Chen et al 1999)] regulate crucial animal cellular functions.…”

Section: Introductionmentioning

confidence: 99%

Effects of cytoplasmic Mg 2+ on slowly activating channels in isolated vacuoles of Beta vulgaris

Carpaneto

Cantù

Gambale

2001

Planta

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The slow vacuolar (SV) channel can mediate a large part of the ionic current in plant tonoplasts, but its actual physiological role is still unclear. We demonstrate that in vacuoles from the taproots of sugar beet (Beta vulgaris L.), besides Ca2+, cytoplasmic Mg2+ also plays an important role in promoting the activation of the SV channel. An increase in Mg2+ concentration decreases the time constants of channel activation and deactivation, and determines a consistent shift, towards negative voltages, of the conductance characteristic; as an example, when the free concentration of Mg2+ was increased from the micromolar range up to 10 mM the activation shifted by about -60 mV. The experimental results obtained, which are based on a fast perfusion procedure allowing us to change the solution bathing the vacuole in a few milliseconds, suggest that magnesium-binding is a faster process than the voltage-activation gating of the channel, which constitutes the rate-limiting step controlling channel opening. Interestingly, the activation of the channel mediated by Mg2+ depends on the cooperative binding of at least three magnesium ions. We verified that cytoplasmic magnesium favours the activation of SV channels in the presence of nanomolar cytoplasmic calcium concentrations. A critical discussion on the Calcium Induced Calcium Release (CICR) mechanism proposed for the SV channel is presented.

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Modulation of calcium‐activated non‐selective cation channel activity by nitric oxide in rat brown adipose tissue.

Cited by 32 publications

References 25 publications

Regulation of the Activity of 27 pS Nonselective Cation Channels in Excised Membrane Patches from Rat Brown-Fat Cells

Regulation of the Activity of 27 pS Nonselective Cation Channels in Excised Membrane Patches from Rat Brown-Fat Cells

Ca 2+ channel inhibition induced by nitric oxide in rat insulinoma RINm5F cells

Effects of cytoplasmic Mg 2+ on slowly activating channels in isolated vacuoles of Beta vulgaris

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