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Готові списки джерел за темами / L-typa calcium channels / Статті в журналах

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Статті в журналах з теми "L-typa calcium channels"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

Collier, M. L., G. Ji, Y. X. Wang, and M. I. Kotlikoff. "Calcium-Induced Calcium Release in Smooth Muscle." Journal of General Physiology 115, no. 5 (2000): 653–62. http://dx.doi.org/10.1085/jgp.115.5.653.

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Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca2+ channels. In heart cells, a tight coupling between the gating of single L-type Ca2+ channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca2+ channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca2+ sparks and propagated Ca2+ waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca2+ channels. L

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2

BIEDA, MARK C., and DAVID R. COPENHAGEN. "N-type and L-type calcium channels mediate glycinergic synaptic inputs to retinal ganglion cells of tiger salamanders." Visual Neuroscience 21, no. 4 (2004): 545–50. http://dx.doi.org/10.1017/s0952523804214055.

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Synaptically localized calcium channels shape the timecourse of synaptic release, are a prominent site for neuromodulation, and have been implicated in genetic disease. In retina, it is well established that L-type calcium channels play a major role in mediating release of glutamate from the photoreceptors and bipolar cells. However, little is known about which calcium channels are coupled to synaptic exocytosis of glycine, which is primarily released by amacrine cells. A recent report indicates that glycine release from spiking AII amacrine cells relies exclusively upon L-type calcium channel

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3

Mangel, A. W., L. Scott, and R. A. Liddle. "Depolarization-stimulated cholecystokinin secretion is mediated by L-type calcium channels in STC-1 cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 2 (1996): G287—G290. http://dx.doi.org/10.1152/ajpgi.1996.270.2.g287.

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To examine the role of calcium channels in depolarization-activated cholecystokinin (CCK) release, studies were performed in an intestinal CCK-secreting cell line, STC-1. Blockade of potassium channels with barium chloride (5 mM) increased the release of CCK by 374.6 +/- 46.6% of control levels. Barium-induced secretion was inhibited by the L-type calcium-channel blocker, nicardipine. Nicardipine (10(-9)-10(-5) M) produced a dose-dependent inhibition in barium-stimulated secretion with a half-maximal inhibition (IC50) value of 0.1 microM. A second L-type calcium-channel blocker, diltiazem (10(

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4

Isaev, Dmytro, Karisa Solt, Oksana Gurtovaya, John P. Reeves, and Roman Shirokov. "Modulation of the Voltage Sensor of L-type Ca2+ Channels by Intracellular Ca2+." Journal of General Physiology 123, no. 5 (2004): 555–71. http://dx.doi.org/10.1085/jgp.200308876.

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Both intracellular calcium and transmembrane voltage cause inactivation, or spontaneous closure, of L-type (CaV1.2) calcium channels. Here we show that long-lasting elevations of intracellular calcium to the concentrations that are expected to be near an open channel (≥100 μM) completely and reversibly blocked calcium current through L-type channels. Although charge movements associated with the opening (ON) motion of the channel's voltage sensor were not altered by high calcium, the closing (OFF) transition was impeded. In two-pulse experiments, the blockade of calcium current and the reducti

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5

Yang, Tingting, Min He, Hailiang Zhang, Paula Q. Barrett, and Changlong Hu. "L- and T-type calcium channels control aldosterone production from human adrenals." Journal of Endocrinology 244, no. 1 (2020): 237–47. http://dx.doi.org/10.1530/joe-19-0259.

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Aldosterone, which plays a key role in the regulation of blood pressure, is produced by zona glomerulosa (ZG) cells of the adrenal cortex. Exaggerated overproduction of aldosterone from ZG cells causes primary hyperaldosteronism. In ZG cells, calcium entry through voltage-gated calcium channels plays a central role in the regulation of aldosterone secretion. Previous studies in animal adrenals and human adrenal adrenocortical cell lines suggest that the T-type but not the L-type calcium channel activity drives aldosterone production. However, recent clinical studies show that somatic mutations

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6

Liu, Xiaoyu, Tingting Yang, Langxi Miao, Yan-Ai Mei, and Changlong Hu. "Leukotriene B4 Inhibits L-Type Calcium Channels via p38 Signaling Pathway in Vascular Smooth Muscle Cells." Cellular Physiology and Biochemistry 37, no. 5 (2015): 1903–13. http://dx.doi.org/10.1159/000438551.

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Background/Aims: Arachidonic acid (AA) and its metabolites are important endogenous lipid messengers. In this study, we test the effect of Leukotriene B4 (LTB4), a 5-lipoxygenase metabolite of AA, on L-type calcium channels in A7r5 rat aortic vascular smooth muscle cells. Methods: L-type calcium channel currents were recorded by a patch-clamp technique. The mRNA expression of CaV1.2 was determined by Real-time RT-PCR. The protein expression of CaV1.2 and p38 activity was determined by Western blot analysis. Results: LTB4 inhibits L-type channel currents in A7r5 cells in a dose-and time- depend

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7

Yarotskyy, Viktor, Guofeng Gao, Blaise Z. Peterson, and Keith S. Elmslie. "Domain III regulates N-type (CaV2.2) calcium channel closing kinetics." Journal of Neurophysiology 107, no. 7 (2012): 1942–51. http://dx.doi.org/10.1152/jn.00993.2011.

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CaV2.2 (N-type) and CaV1.2 (L-type) calcium channels gate differently in response to membrane depolarization, which is critical to the unique physiological functions mediated by these channels. We wondered if the source for these differences could be identified. As a first step, we examined the effect of domain exchange between N-type and L-type channels on activation-deactivation kinetics, which were significantly different between these channels. Kinetic analysis of chimeric channels revealed N-channel-like deactivation for all chimeric channels containing N-channel domain III, while activat

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8

Durante, P., C. G. Cardenas, J. A. Whittaker, S. T. Kitai, and R. S. Scroggs. "Low-Threshold L-type Calcium Channels in Rat Dopamine Neurons." Journal of Neurophysiology 91, no. 3 (2004): 1450–54. http://dx.doi.org/10.1152/jn.01015.2003.

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Ca2+ channel subtypes expressed by dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) were studied using whole cell patch-clamp recordings and blockers selective for different channel types (L, N, and P/Q). Nimodipine (Nim, 2 μM), ω-conotoxin GVIA (Ctx, 1 μM), or ω-agatoxin IVA (Atx, 50 nM) blocked 27, 36, and 37% of peak whole cell Ca2+ channel current, respectively, indicating the presence of L-, N-, and P-type channels. Nim blocked approximately twice as much Ca2+ channel current near activation threshold compared with Ctx or Atx, suggesting that small depolarizations pre

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9

Büschges, A., M. A. Wikström, S. Grillner, and A. El Manira. "Roles of High-Voltage–Activated Calcium Channel Subtypes in a Vertebrate Spinal Locomotor Network." Journal of Neurophysiology 84, no. 6 (2000): 2758–66. http://dx.doi.org/10.1152/jn.2000.84.6.2758.

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Lamprey spinal cord neurons possess N-, L-, and P/Q-type high-voltage–activated (HVA) calcium channels. We have analyzed the role of the different HVA calcium channels subtypes in the overall functioning of the spinal locomotor network by monitoring the influence of their specific agonists and antagonists on synaptic transmission and on N-methyl-d-aspartate (NMDA)–elicited fictive locomotion. The N-type calcium channel blocker ω-conotoxin GVIA (ω-CgTx) depressed synaptic transmission from excitatory and inhibitory interneurons. Blocking L-type and P/Q-type calcium channels with nimodipine and

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10

Rosenberg, R. L., P. Hess, and R. W. Tsien. "Cardiac calcium channels in planar lipid bilayers. L-type channels and calcium-permeable channels open at negative membrane potentials." Journal of General Physiology 92, no. 1 (1988): 27–54. http://dx.doi.org/10.1085/jgp.92.1.27.

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Planar lipid bilayer recordings were used to study Ca channels from bovine cardiac sarcolemmal membranes. Ca channel activity was recorded in the absence of nucleotides or soluble enzymes, over a range of membrane potentials and ionic conditions that cannot be achieved in intact cells. The dihydropyridine-sensitive L-type Ca channel, studied in the presence of Bay K 8644, was identified by a detailed comparison of its properties in artificial membranes and in intact cells. L-type Ca channels in bilayers showed voltage dependence of channel activation and inactivation, open and closed times, an

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11

McCarthy, R. T., C. M. Isales, W. B. Bollag, H. Rasmussen, and P. Q. Barrett. "Atrial natriuretic peptide differentially modulates T- and L-type calcium channels." American Journal of Physiology-Renal Physiology 258, no. 3 (1990): F473—F478. http://dx.doi.org/10.1152/ajprenal.1990.258.3.f473.

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Atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone stimulated by any of these major physiological agonists: angiotensin II, adrenocorticotropic hormone, or K+. The stimulatory actions of each of these agonists depend on calcium influx through voltage-dependent calcium channels. Because two types of calcium channels have been previously described in bovine glomerulosa cells (T- and L-type), the patch-clamp technique was used to evaluate the effect of ANP on each voltage-dependent calcium channel type. ANP was found to differentially modulate these two channel types, stimulat

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12

Taylor, James T., Luping Huang, Brian M. Keyser, Hean Zhuang, Craig W. Clarkson та Ming Li. "Role of high-voltage-activated calcium channels in glucose-regulated β-cell calcium homeostasis and insulin release". American Journal of Physiology-Endocrinology and Metabolism 289, № 5 (2005): E900—E908. http://dx.doi.org/10.1152/ajpendo.00101.2005.

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High-voltage-activated (HVA) calcium channels are known to be the primary source of calcium for glucose-stimulated insulin secretion. However, few studies have investigated how these channels can be regulated by chronically elevated levels of glucose. In the present study, we determined the level of expression of the four major HVA calcium channels (N-type, P/Q-type, LC-type, and LD-type) in rat pancreatic β-cells. Using quantitative real-time PCR (QRT-PCR), we found the expression of all four HVA genes in rat insulinoma cells (INS-1) and in primary isolated rat islet cells. We then determined

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13

Barrett, P. Q., C. M. Isales, W. B. Bollag, and R. T. McCarthy. "Modulation of Ca2+ channels by atrial natriuretic peptide in the bovine adrenal glomerulosa cell." Canadian Journal of Physiology and Pharmacology 69, no. 10 (1991): 1553–60. http://dx.doi.org/10.1139/y91-231.

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In the bovine adrenal glomerulosa cell, calcium influx through voltage-dependent calcium channels is critical to maintaining an aldosterone secretory response. In patch clamp, atrial natriuretic peptide (ANP) inhibits T-type calcium channel current yet stimulates L-type calcium channel current. In the present study the channel effects of ANP observed in the patch-clamp configuration were extended and related to populations of cells. We observed the following. (i) The effect of ANP on T-channel current resulted in the reduction in the open state probability. ANP decreased the mean open state du

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14

Mendelowitz, D., P. J. Reynolds, and M. C. Andresen. "Heterogeneous functional expression of calcium channels at sensory and synaptic regions in nodose neurons." Journal of Neurophysiology 73, no. 2 (1995): 872–75. http://dx.doi.org/10.1152/jn.1995.73.2.872.

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1. In the present study we have taken advantage of the unique anatomy of visceral sensory neurons that enabled us to isolate and examine the role of calcium channel subtypes at the soma, central synaptic terminals, and peripheral sensory endings. 2. N-type calcium channels dominated somatic currents (60%), with lesser (16% and 12%) contributions from P- and L-type channels, respectively, in patch-clamped dispersed nodose neurons using toxins selective for each calcium channel subtype. 3. These toxins also blocked the release of neurotransmitters from these visceral synaptic terminals in a brai

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15

Ouadid-Ahidouch, Halima. "Voltage-gated calcium channels in Pleurodeles oocytes: classification, modulation and functional roles." Zygote 6, no. 1 (1998): 85–95. http://dx.doi.org/10.1017/s0967199400005116.

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SummaryIn unfertilised Pleurodeles oocytes, two distinct types of high voltage-activated Ca2+ channels are expressed: a slowly inactivating Ca2+ channel and a transient one. The first is dihydropyridine-sensitive and is referred to as the L-type Ca2+ channel. The transient channel is highly sensitive to Ni2+. Phosphorylation through protein kinases G and A facilitates and inhibits the L-type Ca2+ channel respectively. The transient type channel is insensitive to stimulation by protein kinases (A and G). The functional expression of L-type and transient Ca2+ channels is modulated by the two mat

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16

Dang, An K., Nathan L. Chaplin, Dilyara A. Murtazina, Ulrich Boehm, Colin M. Clay, and Gregory C. Amberg. "Subplasmalemmal hydrogen peroxide triggers calcium influx in gonadotropes." Journal of Biological Chemistry 293, no. 41 (2018): 16028–42. http://dx.doi.org/10.1074/jbc.ra118.001830.

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Gonadotropin-releasing hormone (GnRH) stimulation of its eponymous receptor on the surface of endocrine anterior pituitary gonadotrope cells (gonadotropes) initiates multiple signaling cascades that culminate in the secretion of luteinizing and follicle-stimulating hormones, which have critical roles in fertility and reproduction. Enhanced luteinizing hormone biosynthesis, a necessary event for ovulation, requires a signaling pathway characterized by calcium influx through L-type calcium channels and subsequent activation of the mitogen-activated protein kinase extracellular signal-regulated k

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17

Manira, A. El, and N. Bussières. "Calcium Channel Subtypes in Lamprey Sensory and Motor Neurons." Journal of Neurophysiology 78, no. 3 (1997): 1334–40. http://dx.doi.org/10.1152/jn.1997.78.3.1334.

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El Manira, A. and N. Bussières. Calcium channel subtypes in lamprey sensory and motor neurons. J. Neurophysiol. 78: 1334–1340, 1997. Pharmacologically distinct calcium channels have been characterized in dissociated cutaneous sensory neurons and motoneurons of the larval lamprey spinal cord. To enable cell identification, sensory dorsal cells and motoneurons were selectively labeled with fluorescein-coupled dextran amine in the intact spinal cord in vitro before dissociation. Calcium channels present in sensory dorsal cells, motoneurons, and other spinal cord neurons were characterized with th

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18

Fieber, L. A., and E. W. McCleskey. "L-type calcium channels in type I cells of the rat carotid body." Journal of Neurophysiology 70, no. 4 (1993): 1378–84. http://dx.doi.org/10.1152/jn.1993.70.4.1378.

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1. Whole-cell and cell-attached patch-clamp recordings were made from enzymatically isolated type I cells from the carotid body of adult rats. Voltage-dependent K+ and Ca2+ channels were observed, but there was no detectable Na+ current. In this respect, rat carotid body cells are unlike those from rabbit, which have Na+ currents and Na(+)-dependent action potentials. 2. The observed Ca2+ channels had the following properties: 1) activation requires voltage steps above -20 mV; 2) little inactivation occurred with holding voltages below -40 mV; 3) one single-channel conductance of 21 pS was fou

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19

Wang, R., E. Karpinski, and P. K. Pang. "Two types of calcium channels in isolated smooth muscle cells from rat tail artery." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (1989): H1361—H1368. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1361.

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Whole cell patch-clamp recordings were carried out on smooth muscle cells from rat tail artery in short-term culture to verify the existence of and to characterize the calcium channels that are present. Two types of voltage-dependent calcium channels were identified in 55 of 63 cells studied. The T-type calcium channel was activated at -50 mV, and the peak inward current occurred at -10 mV, whereas the L-type channel was activated at -20 mV, and the peak inward current occurred at +10 or +20 mV. The T-type channel current inactivated quickly in contrast to the much slower inactivation of the L

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20

Lyford, Greg L., Peter R. Strege, Allan Shepard та ін. "α1C (CaV1.2) L-type calcium channel mediates mechanosensitive calcium regulation". American Journal of Physiology-Cell Physiology 283, № 3 (2002): C1001—C1008. http://dx.doi.org/10.1152/ajpcell.00140.2002.

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Smooth muscle exhibits mechanosensitivity independent of neural input, suggesting that mechanosensitive pathways reside within smooth muscle cells. The native L-type calcium current recorded from human intestinal smooth muscle is modulated by stretch. To define mechanosensitive mechanisms involved in the regulation of smooth muscle calcium entry, we cloned the α1C L-type calcium channel subunit (CaV1.2) from human intestinal smooth muscle and expressed the channel in a heterologous system. This channel subunit retained mechanosensitivity when expressed alone or coexpressed with a β2 calcium ch

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21

Liu, Qi-Yi, and Robert L. Rosenberg. "Stimulation of cardiac L-type calcium channels by extracellular ATP." American Journal of Physiology-Cell Physiology 280, no. 5 (2001): C1107—C1113. http://dx.doi.org/10.1152/ajpcell.2001.280.5.c1107.

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The co-release of ATP with norepinephrine from sympathetic nerve terminals in the heart may augment adrenergic stimulation of cardiac Ca2+ channel activity. To test for a possible direct effect of extracellular ATP on L-type Ca2+ channels, single channels were reconstituted from porcine sarcolemma into planar lipid bilayers so that intracellular signaling pathways could be controlled. Extracellular ATP (2–100 μM) increased the open probability of the reconstituted channels, with a maximal increase of ∼2.6-fold and an EC50 of 3.9 μM. The increase in open probability was due to an increase in ch

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22

Yazaki, I., E. Tosti, and B. Dale. "Cytoskeletal elements link calcium channel activity and the cell cycle in early sea urchin embryos." Development 121, no. 6 (1995): 1827–31. http://dx.doi.org/10.1242/dev.121.6.1827.

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Using the whole-cell clamp technique, we show that L-type calcium channels are activated in early sea urchin blastomeres during M-phase and subsequently inactivated in S-phase. This cyclical channel behaviour occurs in the absence of the nucleus suggesting cytoplasmic regulation independent of the centrosome cycle. Puromycin at 100–400 micromolar does not prevent inactivation of the current showing that this phase, at least, does not require protein synthesis. Cytochalasin B at 2 microgram/ml inhibits the cyclical activity in both M and S phases, while 100 microgram/ml of colchicine inactivate

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23

Rodriguez-Contreras, Adrian, Ping Lv, Jun Zhu, Hyo Jeong Kim, and Ebenezer N. Yamoah. "Effects of Strontium on the Permeation and Gating Phenotype of Calcium Channels in Hair Cells." Journal of Neurophysiology 100, no. 4 (2008): 2115–24. http://dx.doi.org/10.1152/jn.90473.2008.

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To minimize the effects of Ca2+ buffering and signaling, this study sought to examine single Ca2+ channel properties using Sr2+ ions, which substitute well for Ca2+ but bind weakly to intracellular Ca2+ buffers. Two single-channel fluctuations were distinguished by their sensitivity to dihydropyridine agonist (L-type) and insensitivity toward dihydropyridine antagonist (non-L-type). The L- and non-L-type single channels were observed with single-channel conductances of 16 and 19 pS at 70 mM Sr2+ and 11 and 13 pS at 5 mM Sr2+, respectively. We obtained KD estimates of 5.2 and 1.9 mM for Sr2+ fo

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24

Wang, Jijiang, Mustapha Irnaten, and David Mendelowitz. "Agatoxin-IVA-Sensitive Calcium Channels Mediate the Presynaptic and Postsynaptic Nicotinic Activation of Cardiac Vagal Neurons." Journal of Neurophysiology 85, no. 1 (2001): 164–68. http://dx.doi.org/10.1152/jn.2001.85.1.164.

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Whole cell currents and miniature glutamatergic synaptic events (minis) were recorded in vitro from cardiac vagal neurons in the nucleus ambiguus using the patch-clamp technique. We examined whether voltage-dependent calcium channels were involved in the nicotinic excitation of cardiac vagal neurons. Nicotine evoked an inward current, increase in mini amplitude, and increase in mini frequency in cardiac vagal neurons. These responses were inhibited by the nonselective voltage-dependent calcium channel blocker Cd (100 μM). The P-type voltage-dependent calcium channel blocker agatoxin IVA (100 n

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25

Fuchs, Andreas, Marcel Rigaud, Constantine D. Sarantopoulos, Patrick Filip, and Quinn H. Hogan. "Contribution of Calcium Channel Subtypes to the Intracellular Calcium Signal in Sensory Neurons." Anesthesiology 107, no. 1 (2007): 117–27. http://dx.doi.org/10.1097/01.anes.0000267511.21864.93.

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Abstract Background: Although the activation-induced intracellular Ca2+ signal is disrupted by sensory neuron injury, the contribution of specific Ca2+ channel subtypes is unknown. Methods: Transients in dissociated rat dorsal root ganglion neurons were recorded using fura-2 microfluorometry. Neurons from control rats and from neuropathic animals after spinal nerve ligation were activated either by elevated bath K+ or by field stimulation. Transients were compared before and after application of selective blockers of voltage-activated Ca2+ channel subtypes. Results: Transient amplitude and are

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26

Lipscombe, Diane. "L-Type Calcium Channels." Circulation Research 90, no. 9 (2002): 933–35. http://dx.doi.org/10.1161/01.res.0000019740.52306.92.

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27

Triggle, David. "L-Type Calcium Channels." Current Pharmaceutical Design 12, no. 4 (2006): 443–57. http://dx.doi.org/10.2174/138161206775474503.

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28

Hell, J. W., R. E. Westenbroek, C. Warner, et al. "Identification and differential subcellular localization of the neuronal class C and class D L-type calcium channel alpha 1 subunits." Journal of Cell Biology 123, no. 4 (1993): 949–62. http://dx.doi.org/10.1083/jcb.123.4.949.

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To identify and localize the protein products of genes encoding distinct L-type calcium channels in central neurons, anti-peptide antibodies specific for the class C and class D alpha 1 subunits were produced. Anti-CNC1 directed against class C immunoprecipitated 75% of the L-type channels solubilized from rat cerebral cortex and hippocampus. Anti-CND1 directed against class D immunoprecipitated only 20% of the L-type calcium channels. Immunoblotting revealed two size forms of the class C L-type alpha 1 subunit, LC1 and LC2, and two size forms of the class D L-type alpha 1 subunit, LD1 and LD2

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29

Krieger, P., A. Büschges, and A. el Manira. "Calcium Channels Involved in Synaptic Transmission From Reticulospinal Axons in Lamprey." Journal of Neurophysiology 81, no. 4 (1999): 1699–705. http://dx.doi.org/10.1152/jn.1999.81.4.1699.

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Calcium channels involved in synaptic transmission from reticulospinal axons in lamprey. The pharmacology of calcium channels involved in glutamatergic synaptic transmission from reticulospinal axons in the lamprey spinal cord was analyzed with specific agonists and antagonists of different high-voltage activated calcium channels. The N-type calcium channel blocker ω-conotoxin GVIA (ω-CgTx) induced a large decrease of the amplitude of reticulospinal-evoked excitatory postsynaptic potentials (EPSPs). The P/Q-type calcium channel blocker ω-agatoxin IVA (ω-Aga) also reduced the amplitude of the r

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30

Feng, Ming-Guo, Ming Li, and L. Gabriel Navar. "T-type calcium channels in the regulation of afferent and efferent arterioles in rats." American Journal of Physiology-Renal Physiology 286, no. 2 (2004): F331—F337. http://dx.doi.org/10.1152/ajprenal.00251.2003.

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L-type Ca2+ channels predominantly influence preglomerular arterioles, but there is less information regarding the role of T-type Ca2+ channels in regulating the renal microvasculature. We compared the effects of T- and L-type channel blockade on afferent and efferent arterioles using the in vitro blood-perfused juxtamedullary nephron preparation. Single afferent or efferent arterioles of Sprague-Dawley rats were visualized and superfused with solutions containing Ca2+ channel blockers. We confirmed that L-type channel blockade with diltiazem dilates afferent arterioles but has no significant

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31

Friedman, P. A., and F. A. Gesek. "Hormone-responsive Ca2+ entry in distal convoluted tubules." Journal of the American Society of Nephrology 4, no. 7 (1994): 1396–404. http://dx.doi.org/10.1681/asn.v471396.

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This editorial review focuses on recent observations regarding the mechanism and regulation of calcium transport in hormone-sensitive distal convoluted tubules. Parathyroid hormone (PTH) and calcitonin increase active calcium absorption by distal convoluted tubules. Occupancy of these peptide hormone receptors results in the activation of both protein kinase A and protein kinase C. The inhibition of either kinase blocks calcium transport. The time course of stimulation of calcium entry in distal convoluted tubules by PTH is slow compared with that by calcitonin. The latency associated with PTH

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32

Tuana, Balwant S., and Brian J. Murphy. "Biochemical analysis of L-type calcium channels from skeletal and cardiac muscle." Canadian Journal of Physiology and Pharmacology 68, no. 11 (1990): 1482–88. http://dx.doi.org/10.1139/y90-225.

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The development of specific pharmacological agents that modulate different types of ion channels has prompted an extensive effort to elucidate the molecular structure of these important molecules. The calcium channel blockers that specifically modulate the L-type calcium channel activity have aided in the purification and reconstitution of this channel from skeletal muscle transverse tubules. The L-type calcium channel from skeletal muscle is composed of five subunits designated α1, α2, β, γ, and σ. The α1-subunit is the pore-forming polypeptide and contains the ligand binding and phosphorylat

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33

Dolphin, Annette C. "Voltage-gated calcium channels: Their discovery, function and importance as drug targets." Brain and Neuroscience Advances 2 (January 2018): 239821281879480. http://dx.doi.org/10.1177/2398212818794805.

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This review will first describe the importance of Ca2+ entry for function of excitable cells, and the subsequent discovery of voltage-activated calcium conductances in these cells. This finding was rapidly followed by the identification of multiple subtypes of calcium conductance in different tissues. These were initially termed low- and high-voltage activated currents, but were then further subdivided into L-, N-, PQ-, R- and T-type calcium currents on the basis of differing pharmacology, voltage-dependent and kinetic properties, and single channel conductance. Purification of skeletal muscle

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34

Bkaily, Ghassan, Levon Avedanian, Johny Al-Khoury, et al. "Nuclear membrane R-type calcium channels mediate cytosolic ET-1-induced increase of nuclear calcium in human vascular smooth muscle cells." Canadian Journal of Physiology and Pharmacology 93, no. 4 (2015): 291–97. http://dx.doi.org/10.1139/cjpp-2014-0519.

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The objective of this work was to verify whether, as in the case of the plasma membrane of human vascular smooth muscle cells (hVSMCs), cytosolic ET-1-induced increase of nuclear calcium is mediated via the activation of calcium influx through the steady-state R-type calcium channel. Pharmacological tools to identify the R-type calcium channels, as well as real 3-D confocal microscopy imaging techniques coupled to calcium fluorescent probes, were used to study the effect of cytosolic ET-1 on nuclear calcium in isolated nuclei of human hepatocytes and plasma membrane perforated hVSMCs. Our resu

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35

Rosa, Juliana M., Cristina J. Torregrosa-Hetland, Inés Colmena, Luis M. Gutiérrez, Antonio G. García, and Luis Gandía. "Calcium entry through slow-inactivating L-type calcium channels preferentially triggers endocytosis rather than exocytosis in bovine chromaffin cells." American Journal of Physiology-Cell Physiology 301, no. 1 (2011): C86—C98. http://dx.doi.org/10.1152/ajpcell.00440.2010.

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Calcium (Ca2+)-dependent endocytosis has been linked to preferential Ca2+ entry through the L-type (α1D, CaV1.3) of voltage-dependent Ca2+ channels (VDCCs). Considering that the Ca2+-dependent exocytotic release of neurotransmitters is mostly triggered by Ca2+ entry through N-(α1B, CaV2.2) or PQ-VDCCs (α1A, CaV2.1) and that exocytosis and endocytosis are coupled, the supposition that the different channel subtypes are specialized to control different cell functions is attractive. Here we have explored this hypothesis in primary cultures of bovine adrenal chromaffin cells where PQ channels acco

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36

Koenig, Xaver, Lena Rubi, Gerald J. Obermair, et al. "Enhanced currents through L-type calcium channels in cardiomyocytes disturb the electrophysiology of the dystrophic heart." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 4 (2014): H564—H573. http://dx.doi.org/10.1152/ajpheart.00441.2013.

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Duchenne muscular dystrophy (DMD), induced by mutations in the gene encoding for the cytoskeletal protein dystrophin, is an inherited disease characterized by progressive muscle weakness. Besides the relatively well characterized skeletal muscle degenerative processes, DMD is also associated with cardiac complications. These include cardiomyopathy development and cardiac arrhythmias. The current understanding of the pathomechanisms in the heart is very limited, but recent research indicates that dysfunctional ion channels in dystrophic cardiomyocytes play a role. The aim of the present study w

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Syamsunarno, Mas Rizky Anggun Adipurna, Alif Bagus Rakhimullah, Uni Gamayani, et al. "Iron Administration Affects Cardiac Calcium Channel Expression in Mice: The Role of Cardiac Calcium Channel Expression in The Heart of Iron Overload Mice Model." Indonesian Biomedical Journal 12, no. 3 (2020): 261–6. http://dx.doi.org/10.18585/inabj.v12i3.1170.

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BACKGROUND: Iron-overload cardiomyopathy (IOC) is a major comorbidity in patients with chronic repetitive blood transfusion due to myocardial iron uptake that facilitated by calcium channels. As cardiac compensatory mechanism to IOC, we hypothesized the cardiac calcium channels expression would be increased and involved in cardiomyopathy progressivity. This study was aimed to investigate the gene expression of calcium channels in the heart of the iron overload mice model.METHODS: Mice were divided into three groups according to iron administration doses 0, 0.1, and 0.3 mg/day. Systolic blood p

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Wiener, Edith, Roozina Rafique, Arnold Pizzey, Tomas Adejumo, George Chennell, and John B. Porter. "Upregulation of Hepatocellular NTBI Clearance Following Iron Loading Is Associated with Modulation of Membrane T- and L-Type Calcium Channels." Blood 118, no. 21 (2011): 1038. http://dx.doi.org/10.1182/blood.v118.21.1038.1038.

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Abstract Abstract 1038 Background and Rationale. Under conditions of iron overload, the iron binding capacity of transferrin is exceeded and non-transferrin-bound iron (NTBI) species appear in the circulation, at concentrations typically within the range of 0.4–10 μM. NTBI species are rapidly cleared, mainly by the liver but also by the heart and endocrine tissues, causing iron overload of these organs. It is known that pre-loading of hepatocytes or cardiomyocytes with iron causes a paradoxical, dose and time-dependent, increase in NTBI clearance by these cells in vitro through mechanisms that

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39

Strege, Peter R., Cheryl E. Bernard, Yijun Ou, Simon J. Gibbons, and Gianrico Farrugia. "Effect of mibefradil on sodium and calcium currents." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 2 (2005): G249—G253. http://dx.doi.org/10.1152/ajpgi.00022.2005.

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Interstitial cells of Cajal (ICC) generate the electrical slow wave. The ionic conductances that contribute to the slow wave appear to vary among species. In humans, a tetrodotoxin-resistant Na+ current (NaV1.5) encoded by SCN5A contributes to the rising phase of the slow wave, whereas T-type Ca2+ currents have been reported from cultured mouse intestine ICC and also from canine colonic ICC. Mibefradil has a higher affinity for T-type over L-type Ca2+ channels, and the drug has been used in the gastrointestinal tract to identify T-type currents. However, the selectivity of mibefradil for T-typ

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40

Drígeľová, Mária, Bohumila Tarabová, Gunars Duburs, and Ľubica Lacinová. "The dihydropyridine analogue cerebrocrast blocks both T-type and L-type calcium currents." Canadian Journal of Physiology and Pharmacology 87, no. 11 (2009): 923–32. http://dx.doi.org/10.1139/y09-086.

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Cerebrocrast is a novel lipophilic dihydropyridine derivative with potential neuroprotective and antidiabetic properties. We have analyzed its interaction with L-type (CaV1.2b) and T-type (CaV3.1) calcium channels using a whole-cell patch clamp in HEK 293 cells. Cerebrocrast inhibited current flux through both CaV1.2b and CaV3.1 channels. In both cases, the drug was about 10-fold less effective than neutral dihydropyridines, but more efficient than the charged dihydropyridine amlodipine. IC50 values for the CaV1.2b channel were 586 ± 96 nmol/L and 178 ± 78 nmol/L at holding potentials of –80 m

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41

Rodriguez-Tapia, Eileen, Alberto Perez-Medina, Xiaochun Bian, and James J. Galligan. "Upregulation of L-type calcium channels in colonic inhibitory motoneurons of P/Q-type calcium channel-deficient mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 4 (2016): G763—G774. http://dx.doi.org/10.1152/ajpgi.00263.2016.

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Enteric inhibitory motoneurons use nitric oxide and a purine neurotransmitter to relax gastrointestinal smooth muscle. Enteric P/Q-type Ca2+ channels contribute to excitatory neuromuscular transmission; their contribution to inhibitory transmission is less clear. We used the colon from tottering mice ( tg/tg, loss of function mutation in the α1A pore-forming subunit of P/Q-type Ca2+ channels) to test the hypothesis that P/Q-type Ca2+ channels contribute to inhibitory neuromuscular transmission and colonic propulsive motility. Fecal pellet output in vivo and the colonic migrating motor complex

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42

Nikitina, Elena, Ayako Kawashima, Masataka Takahashi, et al. "Alteration in voltage-dependent calcium channels in dog basilar artery after subarachnoid hemorrhage." Journal of Neurosurgery 113, no. 4 (2010): 870–80. http://dx.doi.org/10.3171/2010.2.jns091038.

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Object The L-type Ca++ channel antagonists like nimodipine have limited efficacy against vasospasm after subarachnoid hemorrhage (SAH). The authors tested the hypothesis that this is because SAH alters these channels, rendering them less responsible for contraction. Methods Basilar artery smooth muscle cells were isolated 4, 7, and 21 days after SAH in dogs, and Ca++ channel currents were recorded in 10-mmol/L barium. Proteins for α1 subunits of L-type Ca++ channels were measured by immunoblotting and isometric tension recordings done on rings of the basilar artery. Results High voltage–activa

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43

Haak, Laurel L. "Metabotropic Glutamate Receptor Modulation of Glutamate Responses in the Suprachiasmatic Nucleus." Journal of Neurophysiology 81, no. 3 (1999): 1308–17. http://dx.doi.org/10.1152/jn.1999.81.3.1308.

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Metabotropic glutamate receptor modulation of glutamate responses in the suprachiasmatic nucleus. Glutamate is the primary excitatory transmitter in the suprachiasmatic nucleus (SCN). Ionotropic glutamate receptors (iGluRs) mediate transduction of light information from the retina to the SCN, an important circadian clock phase shifting pathway. Metabotropic glutamate receptors (mGluRs) may play a significant modulatory role. mGluR modulation of SCN responses to glutamate was investigated with fura-2 calcium imaging in SCN explant cultures. SCN neurons showed reproducible calcium responses to g

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44

Rosenberg, R. L., and X. H. Chen. "Characterization and localization of two ion-binding sites within the pore of cardiac L-type calcium channels." Journal of General Physiology 97, no. 6 (1991): 1207–25. http://dx.doi.org/10.1085/jgp.97.6.1207.

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L-type Ca channels from porcine cardiac sarcolemma were incorporated into planar lipid bilayers. We characterized interactions of permeant and blocking ions with the channel's pore by (a) studying the current-voltage relationships for Ca2+ and Na+ when equal concentrations of the ions were present in both internal and external solutions, (b) testing the dose-dependent block of Ba2+ currents through the channels by internally applied cadmium, and (c) examining the dose and voltage dependence of the block of Na+ currents through the channels by internally and externally applied Ca2+. We found th

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45

Gaur, Shikha, Mary E. Morton, G. Peter Frick, and H. Maurice Goodman. "Growth hormone regulates the distribution of L-type calcium channels in rat adipocyte membranes." American Journal of Physiology-Cell Physiology 275, no. 2 (1998): C505—C514. http://dx.doi.org/10.1152/ajpcell.1998.275.2.c505.

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Earlier studies demonstrated that deprivation of growth hormone (GH) for ≥3 h decreased basal and maximally stimulated cytosolic Ca2+ in rat adipocytes and suggested that membrane Ca2+channels might be decreased. Measurement of L-type Ca2+ channels in purified plasma membranes by immunoassay or dihydropyridine binding indicated a two- to fourfold decrease after 3 h of incubation without GH. No such decrease was seen in unfractionated adipocyte membrane preparations. The decrease in plasma membrane channel content was largely accounted for by redistribution of channels to a light microsomal mem

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46

Smith, Carolyn L., Salsabil Abdallah, Yuen Yan Wong, et al. "Evolutionary insights into T-type Ca2+ channel structure, function, and ion selectivity from the Trichoplax adhaerens homologue." Journal of General Physiology 149, no. 4 (2017): 483–510. http://dx.doi.org/10.1085/jgp.201611683.

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Four-domain voltage-gated Ca2+ (Cav) channels play fundamental roles in the nervous system, but little is known about when or how their unique properties and cellular roles evolved. Of the three types of metazoan Cav channels, Cav1 (L-type), Cav2 (P/Q-, N- and R-type) and Cav3 (T-type), Cav3 channels are optimized for regulating cellular excitability because of their fast kinetics and low activation voltages. These same properties permit Cav3 channels to drive low-threshold exocytosis in select neurons and neurosecretory cells. Here, we characterize the single T-type calcium channel from Trich

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47

Seagar, Michael, Christian Lévêque, Nathalie Charvin, et al. "Interactions between proteins implicated in exocytosis and voltage–gated calcium channels." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (1999): 289–97. http://dx.doi.org/10.1098/rstb.1999.0380.

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Neurotransmitter release from synaptic vesicles is triggered by voltage–gated calcium influx through P/Q–type or N–type calcium channels. Purification of N–type channels from rat brain synaptosomes initially suggested molecular interactions between calcium channels and two key proteins implicated in exocytosis: synaptotagmin I and syntaxin 1. Co–immunoprecipitation experiments were consistent with the hypothesis that both N– and P/Q–type calcium channels, but not L–type channels, are associated with the 7S complex containing syntaxin 1, SNAP–25, VAMP and synaptotagmin I or II. Immunofluorescen

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Shah, Kajol, Sarah Seeley, Castin Schulz, Jacqueline Fisher, and Shubha Gururaja Rao. "Calcium Channels in the Heart: Disease States and Drugs." Cells 11, no. 6 (2022): 943. http://dx.doi.org/10.3390/cells11060943.

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Calcium ions are the major signaling ions in the cells. They regulate muscle contraction, neurotransmitter secretion, cell growth and migration, and the activity of several proteins including enzymes and ion channels and transporters. They participate in various signal transduction pathways, thereby regulating major physiological functions. Calcium ion entry into the cells is regulated by specific calcium channels and transporters. There are mainly six types of calcium channels, of which only two are prominent in the heart. In cardiac tissues, the two types of calcium channels are the L type a

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Reuter, H., S. Kokubun, and B. Prod'hom. "Properties and modulation of cardiac calcium channels." Journal of Experimental Biology 124, no. 1 (1986): 191–201. http://dx.doi.org/10.1242/jeb.124.1.191.

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Voltage-dependent calcium channels are widely distributed in excitable membranes and are involved in the regulation of many cellular functions. These channels can be modulated by neurotransmitters and drugs. There is one particular type of calcium channel in cardiac cells (L-type) whose gating is affected in different ways by beta-adrenoceptor and 1,4-dihydropyridine agonists. We have analysed single calcium channel currents (i) in myocytes from rat hearts in the absence and presence of isoproterenol or 8-bromo-cAMP. We have found that both compounds have similar effects on calcium channel pro

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Pérez-García, M. T., T. J. Kamp, and E. Marbán. "Functional properties of cardiac L-type calcium channels transiently expressed in HEK293 cells. Roles of alpha 1 and beta subunits." Journal of General Physiology 105, no. 2 (1995): 289–305. http://dx.doi.org/10.1085/jgp.105.2.289.

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The cardiac dihydropyridine-sensitive calcium channel was transiently expressed in HEK293 cells by transfecting the rabbit cardiac calcium channel alpha 1 subunit (alpha 1C) alone or in combination with the rabbit calcium channel beta subunit cloned from skeletal muscle. Transfection with alpha 1C alone leads to the expression of inward, voltage-activated, calcium or barium currents that exhibit dihydropyridine sensitivity and voltage- as well as calcium-dependent inactivation. Coexpression of the skeletal muscle beta subunit increases current density and the number of high-affinity dihydropyr

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