Nonselective Cation Channels in Brown and White Fat Cells

1993 ◽  
pp. 201-211 ◽  
Author(s):  
Ari Koivisto ◽  
Elisabeth Dotzler ◽  
Ulrich Ruß ◽  
Jan Nedergaard ◽  
Detlef Siemen
Keyword(s):  
Cation Channels ◽  
Fat Cells ◽  
Nonselective Cation Channels ◽  
White Fat

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

1998 ◽  
Vol 8 (5) ◽  
pp. 231-245 ◽  
Author(s):  
Ari Koivisto ◽  
Andreas Klinge ◽  
Jan Nedergaard ◽  
Detlef Siemen
Keyword(s):  
Brown Fat ◽  
Cation Channels ◽  
Fat Cells ◽  
Nonselective Cation Channels

Norepinephrine-induced sustained inward current in brown fat cells: α1-mediated by nonselective cation channels

2000 ◽  
Vol 279 (5) ◽  
pp. E963-E977 ◽  
Author(s):  
Ari Koivisto ◽  
Detlef Siemen ◽  
Jan Nedergaard
Keyword(s):  
Fold Increase ◽  
Brown Fat ◽  
Cation Channels ◽  
Current Response ◽  
Fat Cells ◽  
Adrenergic Stimulation ◽  
Open Probability ◽  
Inward Current ◽  
Nonselective Cation Channels ◽  
Sustained Inward Current

The nature of the sustained norepinephrine-induced depolarization in brown fat cells was examined by patch-clamp techniques. Norepinephrine (NE) stimulation led to a whole cell current response consisting of two phases: a first inward current, lasting for only 1 min, and a sustained inward current, lasting as long as the adrenergic stimulation was maintained. The nature of the sustained current was here investigated. It could be induced by the α1-agonist cirazoline but not by the β3-agonist CGP-12177A. Reduction of extracellular Cl− concentration had no effect, but omission of extracellular Ca2+ or Na+ totally eliminated it. When unstimulated cells were studied in the cell-attached mode, some activity of ≈30 pS nonselective cation channels was observed. NE perfusion led to a 10-fold increase in their open probability (from ≈0.002 to ≈0.017), which persisted as long as the perfusion was maintained. The activation was much stronger with the α1-agonist phenylephrine than with the β3-agonist CGP-12177A, and with the Ca2+ionophore A-23187 than with the adenylyl cyclase activator forskolin. We conclude that the sustained inward current was due to activation of ≈30 pS nonselective cation channels via α1-adrenergic receptors and that the effect may be mediated via an increase in intracellular free Ca2+ concentration.

Chondroid Lipoma, A Tumor of White Fat Cells

1995 ◽  
Vol 19 (11) ◽  
pp. 1272-1276 ◽  
Author(s):  
Gunnlaugur P. Nielsen ◽  
Andrew E. Rosenberg
Keyword(s):  
Fat Cells ◽  
Chondroid Lipoma ◽  
White Fat

Inhibition of hypoxic pulmonary vasoconstriction by antagonists of store-operated Ca2+ and nonselective cation channels

2005 ◽  
Vol 289 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Letitia Weigand ◽  
Joshua Foxson ◽  
Jian Wang ◽  
Larissa A. Shimoda ◽  
J. T. Sylvester
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Cation Channels ◽  
Pulmonary Vasoconstriction ◽  
Nonselective Cation Channels ◽  
Pressor Responses ◽  
Intracellular Ca ◽  
Pulmonary Arterial

Previous studies indicated that acute hypoxia increased intracellular Ca2+ concentration ([Ca2+]i), Ca2+ influx, and capacitative Ca2+ entry (CCE) through store-operated Ca2+ channels (SOCC) in smooth muscle cells from distal pulmonary arteries (PASMC), which are thought to be a major locus of hypoxic pulmonary vasoconstriction (HPV). Moreover, these effects were blocked by Ca2+-free conditions and antagonists of SOCC and nonselective cation channels (NSCC). To test the hypothesis that in vivo HPV requires CCE, we measured the effects of SOCC/NSCC antagonists (SKF-96365, NiCl2, and LaCl3) on pulmonary arterial pressor responses to 2% O2 and high-KCl concentrations in isolated rat lungs. At concentrations that blocked CCE and [Ca2+]i responses to hypoxia in PASMC, SKF-96365 and NiCl2 prevented and reversed HPV but did not alter pressor responses to KCl. At 10 μM, LaCl3 had similar effects, but higher concentrations (30 and 100 μM) caused vasoconstriction during normoxia and potentiated HPV, indicating actions other than SOCC blockade. Ca2+-free perfusate and the voltage-operated Ca2+ channel (VOCC) antagonist nifedipine were potent inhibitors of pressor responses to both hypoxia and KCl. We conclude that HPV required influx of Ca2+ through both SOCC and VOCC. This dual requirement and virtual abolition of HPV by either SOCC or VOCC antagonists suggests that neither channel provided enough Ca2+ on its own to trigger PASMC contraction and/or that during hypoxia, SOCC-dependent depolarization caused secondary activation of VOCC.

scholarly journals Dependence of Spontaneous Electrical Activity and Basal Prolactin Release on Nonselective Cation Channels in Pituitary Lactotrophs

2012 ◽  
pp. 267-275 ◽  
Author(s):  
M. KUČKA ◽  
K. KRETSCHMANNOVÁ ◽  
S. S. STOJILKOVIC ◽  
H. ZEMKOVÁ ◽  
M. TOMIĆ
Keyword(s):  
Electrical Activity ◽  
Action Potentials ◽  
Gh3 Cells ◽  
Cation Channels ◽  
Organic Cations ◽  
Trpc Channels ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Nonselective Cation Channels ◽  
Mrna Transcripts

All secretory anterior pituitary cells fire action potentials spontaneously and exhibit a high resting cation conductance, but the channels involved in the background permeability have not been identified. In cultured lactotrophs and immortalized GH3 cells, replacement of extracellular Na+ with large organic cations, but not blockade of voltage-gated Na+ influx, led to an instantaneous hyperpolarization of cell membranes that was associated with a cessation of spontaneous firing. When cells were clamped at –50 mV, which was close to the resting membrane potential in these cells, replacement of bath Na+ with organic cations resulted in an outward-like current, reflecting an inhibition of the inward holding membrane current and indicating loss of a background-depolarizing conductance. Quantitative RT-PCR analysis revealed the high expression of mRNA transcripts for TRPC1 and much lower expression of TRPC6 in both lactotrophs and GH3 cells. Very low expression of TRPC3, TRPC4, and TRPC5 mRNA transcripts were also present in pituitary but not GH3 cells. 2-APB and SKF-96365, relatively selective blockers of TRPC channels, inhibited electrical activity, Ca2+ influx and prolactin release in a concentration-dependent manner. Gd3+, a common Ca2+ channel blocker, and flufenamic acid, an inhibitor of non-selective cation channels, also inhibited electrical activity, Ca2+ influx and prolactin release. These results indicate that nonselective cation channels, presumably belonging to the TRPC family, contribute to the background depolarizing conductance and firing of action potentials with consequent contribution to Ca2+ influx and hormone release in lactotrophs and GH3 cells.

Effects of calcium on membrane potential and sodium influx in barnacle muscle fibers

1983 ◽  
Vol 244 (3) ◽  
pp. C297-C302 ◽  
Author(s):  
S. S. Sheu ◽  
M. P. Blaustein
Keyword(s):  
Membrane Potential ◽  
Muscle Fibers ◽  
Cation Channels ◽  
Channel Blockers ◽  
Sodium Influx ◽  
Permeable Channel ◽  
Barnacle Muscle ◽  
Nonselective Cation Channels ◽  
Flux Measurements ◽  
Barnacle Muscle Fibers

The influence of internal and external Ca2+ on membrane potential and 22Na influx were tested in internally perfused giant barnacle muscle fibers. The fibers depolarized by about 2-3 mV, and Na+ influx increased when external Ca2+ was removed. These effects were inhibited and reversed by adding 2 mM La3+ externally but not by tetrodotoxin (TTX). Ca2+ channel blockers did not prevent the depolarization. Increasing internal free Ca2+ ([Ca2+]i) from 10(-7) to 10(-5) M also stimulated Na+ influx and depolarized the fibers by a few millivolts. Neither external La3+ nor TTX prevented the effects of raising [Ca2+]i; however, internal tetrabutylammonium ions depolarized the fibers and attenuated the internal Ca2+-dependent effects. These data are consistent with the idea that removal of external Ca2+ activates a La3+-sensitive channel that is permeable to Na+; raising [Ca2+]i activates a La2+-insensitive, Na+-permeable channel that may be similar to the internal Ca2+-activated nonselective cation channels observed in cardiac muscle. The results demonstrate that all Na+ (and Ca2+) fluxes that do not contribute to Na-Ca exchange must be carefully identified before the exchange stoichiometry can be determined from Na+ and Ca2+ flux measurements.

Role of endothelial Ni2+-sensitive Ca2+entry pathway in regulation of EDHF in porcine coronary artery

2001 ◽  
Vol 280 (2) ◽  
pp. H730-H737 ◽  
Author(s):  
Hiroshi Tomioka ◽  
Yuichi Hattori ◽  
Mitsuhiro Fukao ◽  
Hiroshi Watanabe ◽  
Yasuhiro Akaishi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Cyclopiazonic Acid ◽  
Temporal Correlation ◽  
Cation Channels ◽  
Induced Response ◽  
Membrane Hyperpolarization ◽  
Aortic Endothelial Cells ◽  
Porcine Coronary Artery ◽  
Nonselective Cation Channels

Elevation of intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells is proposed to be required for generation of vascular actions of endothelium-derived hyperpolarizing factor (EDHF). This study was designed to determine the endothelial Ca2+ source that is important in development of EDHF-mediated vascular actions. In porcine coronary artery precontracted with U-46619, bradykinin (BK) and cyclopiazonic acid (CPA) caused endothelium-dependent relaxations in the presence of N G-nitro-l-arginine (l-NNA). The l-NNA-resistant relaxant responses were inhibited by high K+, indicating an involvement of EDHF. In the presence of Ni2+, which inhibits Ca2+ influx through nonselective cation channels, the BK-induced EDHF relaxant response was greatly diminished and the CPA-induced response was abolished. BK and CPA elicited membrane hyperpolarization of smooth muscle cells of porcine coronary artery. Ni2+ suppressed the hyperpolarizing responses in a manner analogous to removal of extracellular Ca2+. EDHF-mediated relaxations and hyperpolarizations evoked by BK and CPA in porcine coronary artery showed a temporal correlation with the increases in [Ca2+]i in porcine aortic endothelial cells. The extracellular Ca2+-dependent rises in [Ca2+]i in endothelial cells stimulated with BK and CPA were completely blocked by Ni2+. These results suggest that Ca2+ influx into endothelial cells through nonselective cation channels plays a crucial role in the regulation of EDHF.

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