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Journal articles on the topic 'Ca++-channels blocker'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Lei, Jianzhen, Xiaoxin Liu, Miaomiao Song, et al. "Aberrant Exon 8/8a Splicing by Downregulated PTBP (Polypyrimidine Tract-Binding Protein) 1 Increases Ca V 1.2 Dihydropyridine Resistance to Attenuate Vasodilation." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 10 (2020): 2440–53. http://dx.doi.org/10.1161/atvbaha.120.315010.

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Objective: Calcium channel blockers, such as dihydropyridines, are commonly used to inhibit enhanced activity of vascular Ca V 1.2 channels in hypertension. However, patients who are insensitive to such treatments develop calcium channel blocker-resistant hypertension. The function of Ca V 1.2 channel is diversified by alternative splicing, and the splicing factor PTBP (polypyrimidine tract-binding protein) 1 influences the utilization of mutually exclusive exon 8/8a of the Ca V 1.2 channel during neuronal development. Nevertheless, whether and how PTBP1 makes a role in the calcium channel blo

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2

Nagayama, Takahiro, Kimiya Masada, Makoto Yoshida, et al. "Role of K+ channels in adrenal catecholamine secretion in anesthetized dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 4 (1998): R1125—R1130. http://dx.doi.org/10.1152/ajpregu.1998.274.4.r1125.

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We examined the role of K+ channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K+ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K+ channel (KA type) blocker mast cell degranulating (MCD) peptide infusion (10–100 ng/min) enhanced increases in CA output induced by SNS (1–3 Hz), but it did not affect increases in CA output induced by ACh (0.75–3 μg), DMPP (0.

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3

Neyton, J., and M. Pelleschi. "Multi-ion occupancy alters gating in high-conductance, Ca(2+)-activated K+ channels." Journal of General Physiology 97, no. 4 (1991): 641–65. http://dx.doi.org/10.1085/jgp.97.4.641.

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In this study, single-channel recordings of high-conductance Ca(2+)-activated K+ channels from rat skeletal muscle inserted into planar lipid bilayer were used to analyze the effects of two ionic blockers, Ba2+ and Na+, on the channel's gating reactions. The gating equilibrium of the Ba(2+)-blocked channel was investigated through the kinetics of the discrete blockade induced by Ba2+ ions. Gating properties of Na(+)-blocked channels could be directly characterized due to the very high rates of Na+ blocking/unblocking reactions. While in the presence of K+ (5 mM) in the external solution Ba2+ i

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4

Wilkinson, M. F., and S. Barnes. "The dihydropyridine-sensitive calcium channel subtype in cone photoreceptors." Journal of General Physiology 107, no. 5 (1996): 621–30. http://dx.doi.org/10.1085/jgp.107.5.621.

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High-voltage activated Ca channels in tiger salamander cone photoreceptors were studied with nystatin-permeabilized patch recordings in 3 mM Ca2+ and 10 mM Ba2+. The majority of Ca channel current was dihydropyridine sensitive, suggesting a preponderance of L-type Ca channels. However, voltage-dependent, incomplete block (maximum 60%) by nifedipine (0.1-100 microM) was evident in recordings of cones in tissue slice. In isolated cones, where the block was more potent, nifedipine (0.1-10 microM) or nisoldipine (0.5-5 microM) still failed to eliminate completely the Ca channel current. Nisoldipin

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5

Blundon, J. A., S. N. Wright, M. S. Brodwick, and G. D. Bittner. "Presynaptic calcium-activated potassium channels and calcium channels at a crayfish neuromuscular junction." Journal of Neurophysiology 73, no. 1 (1995): 178–89. http://dx.doi.org/10.1152/jn.1995.73.1.178.

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1. We used a two-microelectrode current clamp to investigate various characteristics of the Ca(2+)-activated K+ conductance [gK(Ca)] and Ca2+ conductance (gCa), and transmitter release in presynaptic terminals of excitatory neuromuscular junctions in the crayfish walking leg. 2. Voltage-activated Na+ conductances (gNa) and K+ conductances [gK(v)] were blocked with tetrodotoxin and 3,4-diaminopyridine, respectively. Under these conditions, presynaptic depolarization produced by a first (conditioning) pulse admitted Ca2+ into the presynaptic terminals and activated gK(Ca), which modulated the am

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6

Kamishima, T., M. T. Nelson, and J. B. Patlak. "Carbachol modulates voltage sensitivity of calcium channels in bronchial smooth muscle of rats." American Journal of Physiology-Cell Physiology 263, no. 1 (1992): C69—C77. http://dx.doi.org/10.1152/ajpcell.1992.263.1.c69.

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The role of voltage-dependent Ca channels in carbachol (CCh)-induced contraction of rat bronchus was investigated. Membrane depolarization and BAY K 8644, a Ca channel opener, significantly enhanced CCh-induced contractions. Nisoldipine, an organic Ca channel blocker, significantly inhibited the contractions. Cadmium, an inorganic Ca channel blocker, completely inhibited maintained contractions caused by CCh. These results suggested that the voltage-dependent Ca channels play an important role in sustained cholinergic contractions. This hypothesis was tested further by investigating the proper

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7

Smith, Forrest L., Richard W. Davis, and Richard Carter. "Influence of Voltage-sensitive Ca++Channel Drugs on Bupivacaine Infiltration Anesthesia in Mice." Anesthesiology 95, no. 5 (2001): 1189–97. http://dx.doi.org/10.1097/00000542-200111000-00024.

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Background Local anesthesia has been traditionally associated with blockade of voltage-sensitive sodium (Na(+)) channels. Yet in vitro evidence indicates that local anesthetic mechanisms are more complex than previously understood. For example, local anesthetics bind and allosterically modify 1,4-dihydropyridine-sensitive Ca(++) channels and can reduce Ca(++) influx in tissues. The current study examines the influence of voltage-sensitive Ca(++) channels in bupivacaine infiltration anesthesia. Methods Baseline tail-flick latencies to radiant heat nociception were obtained before subcutaneous i

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8

McCann, J. D., and M. J. Welsh. "Neuroleptics antagonize a calcium-activated potassium channel in airway smooth muscle." Journal of General Physiology 89, no. 2 (1987): 339–52. http://dx.doi.org/10.1085/jgp.89.2.339.

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We examined the effect of neuroleptics on Ca-activated K channels from dog airway smooth muscle cells. Because these agents inhibit a variety of other Ca-mediated processes, it seemed possible that they might also inhibit Ca-activated K channels. In excised, inside-out patches, several neuroleptics potently and reversibly inhibited the K channel from the internal but not the external surface of the patch. Measurements of the effect on open probability and open- and closed-state durations support a simple kinetic model in which neuroleptics bind to and block the open channel. Inhibition by neur

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9

Moore, Christopher L., Samantha J. McClenahan, Hillary M. Hanvey, et al. "Beta1-Adrenergic Receptor-Mediated Dilation of Rat Cerebral Artery Requires Shaker-Type KV1 Channels on PSD95 Scaffold." Journal of Cerebral Blood Flow & Metabolism 35, no. 9 (2015): 1537–46. http://dx.doi.org/10.1038/jcbfm.2015.91.

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Postsynaptic density-95 (PSD95) is a scaffolding protein in cerebral vascular smooth muscle cells (cVSMCs), which binds to Shaker-type K+ (KV1) channels and facilitates channel opening through phosphorylation by protein kinase A. β1-Adrenergic receptors (β1ARs) also have a binding motif for PSD95. Functional association of β1AR with KV1 channels through PSD95 may represent a novel vasodilator complex in cerebral arteries (CA). We explored whether a β1AR-PSD95-KV1 complex is a determinant of rat CA dilation. RT-PCR and western blots revealed expression of β1AR in CA. Isoproterenol induced a con

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10

Meguro, Toshinari, Christoph P. R. Klett, Betty Chen, Andrew D. Parent, and John H. Zhang. "Role of calcium channels in oxyhemoglobin-induced apoptosis in endothelial cells." Journal of Neurosurgery 93, no. 4 (2000): 640–46. http://dx.doi.org/10.3171/jns.2000.93.4.0640.

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Object. Oxyhemoglobin (OxyHb) released from hemolysed erythrocytes has been considered to be responsible for cerebral vasospasm after subarachnoid hemorrhage. The authors previously reported that OxyHb produced apoptosis in cultured vascular endothelial cells. The change in intracellular Ca++ homeostasis was expected to be one of the possible mechanisms of the cytotoxic effects of OxyHb. This study was undertaken to investigate the protective effects of Ca++-channel blockers on OxyHb-induced apoptosis.Methods. Cultured bovine coronary artery and brain microvascular endothelial cells (passages

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11

Najibi, S., and R. A. Cohen. "Enhanced role of K+ channels in relaxations of hypercholesterolemic rabbit carotid artery to NO." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 3 (1995): H805—H811. http://dx.doi.org/10.1152/ajpheart.1995.269.3.h805.

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Endothelium-dependent relaxations to acetylcholine remain normal in the carotid artery of hypercholesterolemic rabbits, but unlike endothelium-dependent relaxations of normal rabbits, they are inhibited by charybdotoxin, a specific blocker of Ca(2+)-dependent K+ channels. Because nitric oxide (NO) is the mediator of endothelium-dependent relaxation and can activate Ca(2+)-dependent K+ channels directly or via guanosine 3',5'-cyclic monophosphate, the present study investigated the role of Ca(2+)-dependent K+ channels in relaxations caused by NO, sodium nitroprusside, and 8-bromoguanosine 3',5'

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12

Wang, X., T. Inukai, M. A. Greer, and S. E. Greer. "Rat Prl and TSH secretion are regulated differently by K(+)-channel blockers." American Journal of Physiology-Endocrinology and Metabolism 266, no. 1 (1994): E39—E43. http://dx.doi.org/10.1152/ajpendo.1994.266.1.e39.

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All four different K(+)-channel blockers [tetraethylammonium (TEA), a nonselective K(+)-channel blocker; tolbutamide, an ATP-sensitive K(+)-channel blocker; quinine and 4-aminopyridine, both primarily voltage-dependent K(+)-channel blockers] stimulated prolactin (Prl) secretion by acutely dispersed anterior pituitary cells but had no effect on thyroid-stimulating hormone (TSH) secretion. TEA stimulated Prl secretion in a dose-dependent manner between 1 microM and 20 mM, but even as high as 20 mM, TEA did not induce TSH secretion. Valinomycin (2 microM), a K+ ionophore, inhibited both basal and

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13

Cohen, C. J., S. Spires, and D. Van Skiver. "Block of T-type Ca channels in guinea pig atrial cells by antiarrhythmic agents and Ca channel antagonists." Journal of General Physiology 100, no. 4 (1992): 703–28. http://dx.doi.org/10.1085/jgp.100.4.703.

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Myocardial cells have two types of Ca channels commonly called T-type and L-type. Whole cell Ca channel currents in guinea pig atrial myocytes can be separated and quantitated by analyzing channel closing kinetics after a brief depolarization (tail current analysis). L-type Ca channels deactivate rapidly when the membrane is repolarized and T-type Ca channels deactivate relatively slowly. Ca channel block by the therapeutically useful Ca channel antagonists is voltage dependent, so it is desirable to study block of both channel types over an extended voltage range. Tail current analysis allows

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14

Gilbert, Robert, Jennifer S. Ryan, Magda Horackova, Frank M. Smith, and Melanie E. M. Kelly. "Actions of substance P on membrane potential and ionic currents in guinea pig stellate ganglion neurons." American Journal of Physiology-Cell Physiology 274, no. 4 (1998): C892—C903. http://dx.doi.org/10.1152/ajpcell.1998.274.4.c892.

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Neuropeptides are known to modulate the excitability of mammalian sympathetic neurons by their actions on various types of K+ and Ca2+ channels. We used whole cell patch-clamp recording methods to study the actions of substance P (SP) on dissociated adult guinea pig stellate ganglion (SG) neurons. Under current-clamp conditions, SG neurons exhibited overshooting action potentials followed by afterhyperpolarizations (AHP). The K+ channel blocker tetraethylammonium (1 mM), the Ca2+ channel blocker Cd2+ (0.1–0.2 mM), and SP (500 nM) depolarized SG neurons, decreased the AHP amplitude, and increas

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15

Carl, A., B. W. Frey, S. M. Ward, K. M. Sanders, and J. L. Kenyon. "Inhibition of slow-wave repolarization and Ca(2+)-activated K+ channels by quaternary ammonium ions." American Journal of Physiology-Cell Physiology 264, no. 3 (1993): C625—C631. http://dx.doi.org/10.1152/ajpcell.1993.264.3.c625.

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We studied the effects of the K+ channel blocker tetrapentylammonium (TPeA) on the electrical activity of intact circular smooth muscle from canine colon. TPeA (10 and 20 microM) increased slow-wave duration and "locked" the membrane potential around -30 mV plateau potential after several minutes of application, suggesting that K+ channels are essential for termination of colonic slow waves. Repolarization and normal slow-wave activity resumed after 20-30 min of washout. The patch-clamp technique was used to study the block of large-conductance Ca(2+)-activated K+ channels (BK channels) by TPe

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16

Pappone, P. A., and M. T. Lucero. "Potassium channel block does not affect metabolic responses of brown fat cells." American Journal of Physiology-Cell Physiology 262, no. 3 (1992): C678—C681. http://dx.doi.org/10.1152/ajpcell.1992.262.3.c678.

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Hormonally stimulated brown fat cells are capable of extremely high metabolic rates, making them an excellent system in which to examine the role of plasma membrane ion channels in cell metabolism. We have previously shown that brown fat cell membranes have both voltage-gated and calcium-activated potassium channels (Voltage-gated potassium channels in brown fat cells. J. Gen. Physiol. 93: 451-472, 1989; Membrane responses to norepinephrine in cultured brown fat cells. J. Gen. Physiol. 95: 523-544, 1990). Currents through both the voltage-activated potassium channels, IK,V, and the calcium-act

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17

Mehrke, G., X. G. Zong, V. Flockerzi, and F. Hofmann. "The Ca(++)-channel blocker Ro 40-5967 blocks differently T-type and L-type Ca++ channels." Journal of Pharmacology and Experimental Therapeutics 271, no. 3 (1994): 1483–88. https://doi.org/10.1016/s0022-3565(25)24034-4.

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18

Corrales, Alexandra, Fang Xu, Zayra V. Garavito-Aguilar, Thomas J. J. Blanck, and Esperanza Recio-Pinto. "Isoflurane Reduces the Carbachol-evoked Ca2+Influx in Neuronal Cells." Anesthesiology 101, no. 4 (2004): 895–901. http://dx.doi.org/10.1097/00000542-200410000-00014.

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Background The authors previously reported that the isoflurane-caused reduction of the carbachol-evoked cytoplasmic Ca transient increase ([Ca]cyt) was eliminated by K or caffeine-pretreatment. In this study the authors investigated whether the isoflurane-sensitive component of the carbachol-evoked [Ca]cyt transient involved Ca influx through the plasma membrane. Methods Perfused attached human neuroblastoma SH-SY5Y cells were exposed to carbachol (1 mm, 2 min) in the absence and presence of isoflurane (1 mm) and in the absence and presence of extracellular Ca (1.5 mm). The authors studied the

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19

Lansman, J. B., P. Hess, and R. W. Tsien. "Blockade of current through single calcium channels by Cd2+, Mg2+, and Ca2+. Voltage and concentration dependence of calcium entry into the pore." Journal of General Physiology 88, no. 3 (1986): 321–47. http://dx.doi.org/10.1085/jgp.88.3.321.

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We studied the blocking actions of external Ca2+, Mg2+, Ca2+, and other multivalent ions on single Ca channel currents in cell-attached patch recordings from guinea pig ventricular cells. External Cd or Mg ions chopped long-lasting unitary Ba currents promoted by the Ca agonist Bay K 8644 into bursts of brief openings. The bursts appear to arise from discrete blocking and unblocking transitions. A simple reaction between a blocking ion and an open channel was suggested by the kinetics of the bursts: open and closed times within a burst were exponentially distributed, the blocking rate varied l

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20

Angermann, Jeff E., Abigail S. Forrest, Iain A. Greenwood, and Normand Leblanc. "Activation of Ca2+-activated Cl– channels by store-operated Ca2+ entry in arterial smooth muscle cells does not require reverse-mode Na+/Ca2+ exchange." Canadian Journal of Physiology and Pharmacology 90, no. 7 (2012): 903–21. http://dx.doi.org/10.1139/y2012-081.

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The main purpose of this study was to characterize the stimulation of Ca2+-activated Cl– (ClCa) by store-operated Ca2+ entry (SOCE) channels in rabbit pulmonary arterial smooth muscle cells (PASMCs) and determine if this process requires reverse-mode Na+/Ca2+ exchange (NCX). In whole-cell voltage clamped PASMCs incubated with 1 μmol/L nifedipine (Nif) to inhibit Ca2+ channels, 30 μmol/L cyclopiazonic acid (CPA), a SERCA pump inhibitor, activated a nonselective cation conductance permeable to Na+ (ISOC) during an initial 1–3 s step, ranging from–120 to +60 mV, and Ca2+-activated Cl– current (IC

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Floyd, Rachel V., Craig Winstanley, Ali Bakran, Susan Wray, and Theodor V. Burdyga. "Modulation of ureteric Ca signaling and contractility in humans and rats by uropathogenic E. coli." American Journal of Physiology-Renal Physiology 298, no. 4 (2010): F900—F908. http://dx.doi.org/10.1152/ajprenal.00468.2009.

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Ascending urinary tract infections, a significant cause of kidney damage, are predominantly caused by uropathogenic Escherichia coli (UPEC). However, the role and mechanism of changes in ureteric function during infection are poorly understood. We therefore investigated the effects of UPEC on Ca signaling and contractions in rat ( n = 17) and human ( n = 6) ureters. Ca transients and force were measured and effects of UPEC on the urothelium were monitored in live tissues. In both species, luminal exposure of ureters to UPEC strains J96 and 536 caused significant time-dependent decreases in pha

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22

Sato, K., and N. Suzuki. "The contribution of a Ca(2+)-activated Cl(−) conductance to amino-acid-induced inward current responses of ciliated olfactory neurons of the rainbow trout." Journal of Experimental Biology 203, no. 2 (2000): 253–62. http://dx.doi.org/10.1242/jeb.203.2.253.

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To determine whether amino-acid-induced inward currents of ciliated olfactory receptor neurons (ORNs) in rainbow trout (Oncorhynchus mykiss) include a Ca(2+)-activated Cl(−) conductance, we first studied changes in reversal potential and the current/voltage relationships of the responses of ORNs to an amino acid mixture (l-alanine, l-arginine, l-glutamate and l-norvaline; all 10 mmol l(−)(1)) with different concentrations of Na(+) and Cl(−) in the perfusion and recording pipette solutions. We also examined the effects of six different Cl(−) channel blockers on the responses of ORNs using a con

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23

Li, X., and D. J. Bennett. "Apamin-Sensitive Calcium-Activated Potassium Currents (SK) Are Activated by Persistent Calcium Currents in Rat Motoneurons." Journal of Neurophysiology 97, no. 5 (2007): 3314–30. http://dx.doi.org/10.1152/jn.01068.2006.

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Low voltage–activated persistent inward calcium currents (Ca PICs) occur in rat motoneurons and are mediated by Cav1.3 L-type calcium channels (L-Ca current). The objectives of this paper were to determine whether this L-Ca current activates a sustained calcium-activated potassium current (SK current) and examine how such SK currents change with spinal injury. For comparison, the SK current that produces the postspike afterhyperpolarization (mAHP) was also quantified. Intracellular recordings were made from motoneurons of adult acute and chronic spinal rats while the whole sacrocaudal spinal c

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24

Hempelmann, Ralf G., Jörg Seebeck, Albrecht Ziegler, and H. Maximilian Mehdorn. "Effects of potassium channel inhibitors on the relaxation induced by the NO donor DEA/NO in isolated human cerebral arteries." Journal of Neurosurgery 93, no. 6 (2000): 1048–54. http://dx.doi.org/10.3171/jns.2000.93.6.1048.

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Object. The goal of this study was to investigate whether K+ channels are involved in nitric oxide (NO)—induced relaxation of isolated human cerebral arteries.Methods. Successive concentration—response curves relating to the use of the NO donor diethylamine NO (DEA/NO) were established in the absence and presence of different K+ channel inhibitors after mounting human cerebral arteries onto a wire myograph. The arteries were obtained from macroscopically intact tissue that had been removed during brain tumor operations.A high K+ concentration partially inhibited the relaxant effects of DEA/NO.

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25

Sidell, N., L. C. Schlichter, S. C. Wright, S. Hagiwara, and S. H. Golub. "Potassium channels in human NK cells are involved in discrete stages of the killing process." Journal of Immunology 137, no. 5 (1986): 1650–58. http://dx.doi.org/10.4049/jimmunol.137.5.1650.

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Abstract Using the whole-cell variation of the patch-clamp technique, we have found a voltage-dependent K+ current in human natural killer (NK) cells. This K+ current is reduced in a dose-dependent manner by a variety of ion-channel blockers (verapamil, quinidine, 4-aminopyridine, Cd2+) at concentrations comparable to those that inhibit natural killing. Pretreatment of target cells with quinidine or verapamil did not significantly reduce their sensitivity to killing, whereas substantial inhibition of killing was observed after pretreatment of effector cells. Both verapamil and quinidine reduce

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26

Scherubl, H., T. Kleppisch, A. Zink, F. Raue, D. Krautwurst, and J. Hescheler. "Major role of dihydropyridine-sensitive Ca2+ channels in Ca(2+)-induced calcitonin secretion." American Journal of Physiology-Endocrinology and Metabolism 264, no. 3 (1993): E354—E360. http://dx.doi.org/10.1152/ajpendo.1993.264.3.e354.

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Endocrine cells are known to possess multiple types of Ca2+ channels. In neurons, omega-conotoxin-sensitive N-type Ca2+ channels have been shown to play a dominant role in neurotransmitter release, but uncertainty remains about the types of Ca2+ channels involved in stimulus-secretion coupling in endocrine cells. We investigated the relative contribution of 1,4-dihydropyridine-sensitive and omega-conotoxin-sensitive Ca2+ channels to Ca(2+)-induced calcitonin release in parafollicular cells of the thyroid (C cells). In whole cell voltage-clamp experiments, both 1,4-dihydropyridine-sensitive and

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Sorokina, D. M., I. F. Shaidullov, D. Buchareb, F. G. Sitdikov, and G. F. Sitdikova. "Effect of Hydrogen Sulphide on Spontaneous Contractions of the Rat Jejunum. Role of K<sub>V</sub>-, K<sub>Ca</sub>-, and K<sub>ir</sub>-Channels." Биологические мембраны Журнал мембранной и клеточной биологии 40, no. 6 (2023): 432–42. http://dx.doi.org/10.31857/s0233475523060099.

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In this work, we analyzed the role of voltage-gated (KV), calcium-activated (KCa), and inward-rectifier potassium channels (Kir) in the effects of hydrogen sulphide (H2S) donor sodium hydrosulphide (NaHS) on the spontaneous contractile activity of the rat jejunum. Experiments were performed on jejunum segments under isometric contraction conditions. It was shown that NaHS reduced the basal tension of the segments, the amplitude, and the frequency of spontaneous contractions in a dose-dependent manner (10–500 μM); the half-effective concentration (EC50) of the inhibitory effect of NaHS on ampli

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Barman, S. A. "Pulmonary vasoreactivity to endothelin-1 at elevated vascular tone is modulated by potassium channels." Journal of Applied Physiology 80, no. 1 (1996): 91–98. http://dx.doi.org/10.1152/jappl.1996.80.1.91.

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The role of K+ channels on the pressor effect of endothelin-1 (ET-1) on vascular resistance and compliance in the canine pulmonary circulation was studied by using three different K+ channel inhibitors in isolated blood-perfused dog lungs when vascular tone was elevated with U-46619: 1) 10(-6) M glibenclamide, a potent and selective blocker of ATP-sensitive K+ channels; 2) 1 mM tetraethylammonium ions (TEA), an inhibitor of Ca(2+)-dependent K+ channels; and 3) 10(-4) M 4-aminopyridine, a nonspecific inhibitor of K+ channels. The results of the present study showed that under control vascular t

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Geary, G. G., D. N. Krause, and S. P. Duckles. "Melatonin directly constricts rat cerebral arteries through modulation of potassium channels." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 3 (1997): H1530—H1536. http://dx.doi.org/10.1152/ajpheart.1997.273.3.h1530.

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The pineal hormone melatonin was found to decrease luminal diameter of rat middle cerebral artery segments, pressurized in vitro, in a concentration-dependent manner (concentration that produced a half-maximal effect = 2.7 nM). Contractile responses to melatonin were inhibited by luzindole, a melatonin receptor antagonist, but not by the serotonin receptor antagonist ketanserin. Pertussis toxin abolished the effect of melatonin, which is consistent with involvement of Gi or G(o) protein-coupled receptors. The maximal effect of melatonin was increased by elevating transmural pressure. When comp

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Scholz, K. P., and R. J. Miller. "Presynaptic inhibition at excitatory hippocampal synapses: development and role of presynaptic Ca2+ channels." Journal of Neurophysiology 76, no. 1 (1996): 39–46. http://dx.doi.org/10.1152/jn.1996.76.1.39.

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1. Presynaptic inhibition of excitatory postsynaptic currents (EPSCs) induced by activation of adenosine receptors was examined at hippocampal synapses in cell culture. Changes in the degree of presynaptic inhibition during development were examined. The results were then used to test the role of presynaptic Ca2+ channels in presynaptic inhibition. 2. Application of the selective A1 adenosine receptor agonist N6-cyclopentyladenosine (CPA) reduced EPSCs measured with the use of whole cell voltage-clamp procedures. In cells grown in culture for < 15 days, CPA (100 nM) inhibited EPSCs by 74 +/

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Yarotskyy, Viktor, та Keith S. Elmslie. "ω-Conotoxin GVIA Alters Gating Charge Movement of N-Type (CaV2.2) Calcium Channels". Journal of Neurophysiology 101, № 1 (2009): 332–40. http://dx.doi.org/10.1152/jn.91064.2008.

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ω-conotoxin GVIA (ωCTX) is a specific blocker of N-type calcium (CaV2.2) channels that inhibits neuropathic pain. While the toxin appears to be an open channel blocker, we show that N-channel gating charge movement is modulated. Gating currents were recorded from N-channels expressed along with ß2a and α2δ subunits in HEK293 cells in external solutions containing either lanthanum and magnesium (La-Mg) or 5 mM Ca2+ plus ωCTX (ωCTX-Ca). A comparison showed that ωCTX induced a 10-mV right shift in the gating charge versus voltage ( Q- V) relationship, smaller off-gating current time constant (τ Q

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Hong, K. W., S. E. Yoo, S. S. Yu, J. Y. Lee, and B. Y. Rhim. "Pharmacological coupling and functional role for CGRP receptors in the vasodilation of rat pial arterioles." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 1 (1996): H317—H323. http://dx.doi.org/10.1152/ajpheart.1996.270.1.h317.

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In this study, we investigated the signal transduction underlying the vasodilator action of calcitonin gene-related peptide (CGRP) in the rat pial arterioles. In an in vivo experiment, changes in pial arterial diameters (20.2 +/- 1.9 microns) were observed under suffusion with mock cerebrospinal fluid containing CGRP (10(-9)-10(-7) M) directly through a closed cranial window. Changes in intracellular adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in response to CGRP and levcromakalim were measured in the pial arterioles in an in vitro experiment. CGRP-induced vasodilation and cAMP pr

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Gregerson, K. A., R. Chuknyiska, and N. Golesorkhi. "Stimulation of prolactin release by dopamine withdrawal: role of calcium influx." American Journal of Physiology-Endocrinology and Metabolism 267, no. 5 (1994): E789—E794. http://dx.doi.org/10.1152/ajpendo.1994.267.5.e789.

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Withdrawal of dopamine (DA), a neurotransmitter that inhibits prolactin (PRL) release from the anterior pituitary, stimulates PRL release with transient (30- to 45-min) secretory rates that exceed those observed before application of DA ("PRL rebound"). Using patch-clamp methods on identified rat lactotropes, we have demonstrated that a period of increased Ca(2+)-spiking activity follows recovery from the DA-induced hyperpolarization. The present experiments used dissociated pituitary cells to identify the relative roles of adenosine 3',5'-cyclic monophosphate (cAMP), inositol phosphates, and

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34

Furutani, Kenta, Miho Ikoma, Hideaki Ishii, Hiroshi Baba, and Tatsuro Kohno. "Bupivacaine Inhibits Glutamatergic Transmission in Spinal Dorsal Horn Neurons." Anesthesiology 112, no. 1 (2010): 138–43. http://dx.doi.org/10.1097/01.anes.0000365964.97138.9a.

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Background The local anesthetic bupivacaine is thought not only to block sodium channels but also to interact with various receptors. Here, the authors focus on excitatory glutamatergic transmission in the superficial dorsal horn of the spinal cord with respect to its importance for nociceptive processing. Methods The effects of bupivacaine on the response to exogenous administration of N-methyl-D-aspartate (NMDA) receptor agonists were examined in lamina II neurons of adult rat spinal cord slices using the whole-cell patch-clamp technique. Results Bupivacaine (0.5, 2 mm) dose-dependently redu

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Barnes, S., and M. C. Deschenes. "Contribution of Ca and Ca-activated Cl channels to regenerative depolarization and membrane bistability of cone photoreceptors." Journal of Neurophysiology 68, no. 3 (1992): 745–55. http://dx.doi.org/10.1152/jn.1992.68.3.745.

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1. Cone photoreceptors in several vertebrate species generate Ca-dependent regenerative depolarizations (e.g., Ca spikes lasting up to 2 s) in response to current injection or surround illumination and may remain in a state of prolonged depolarization (e.g., a permanent plateau near 0 mV) after these stimuli. This paper, while confirming the role of Ca channels in the regenerative depolarization, demonstrates that Ca-activated Cl channels either enhance or hinder prolonged depolarization, depending on the value of the chloride equilibrium potential (ECl). 2. Current- and voltage-clamp recordin

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Oshima-Takago, Tomoko, and Hideki Takago. "NMDA receptor-dependent presynaptic inhibition at the calyx of Held synapse of rat pups." Open Biology 7, no. 7 (2017): 170032. http://dx.doi.org/10.1098/rsob.170032.

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N -Methyl- d -aspartate receptors (NMDARs) play diverse roles in synaptic transmission, synaptic plasticity, neuronal development and neurological diseases. In addition to their postsynaptic expression, NMDARs are also expressed in presynaptic terminals at some central synapses, and their activation modulates transmitter release. However, the regulatory mechanisms of NMDAR-dependent synaptic transmission remain largely unknown. In the present study, we demonstrated that activation of NMDARs in a nerve terminal at a central glutamatergic synapse inhibits presynaptic Ca 2+ currents (I Ca ) in a

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Nilius, B., J. Sehrer, S. Heinke, and G. Droogmans. "Ca2+ release and activation of K+ and Cl- currents by extracellular ATP in distal nephron epithelial cells." American Journal of Physiology-Cell Physiology 269, no. 2 (1995): C376—C384. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c376.

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We have measured ionic currents and changes in intracellular Ca2+ concentration ([Ca2+]i) induced by extracellular ATP in single epithelial cells of the distal nephron from toad (A6 cells). ATP increased [Ca2+]i and concomitantly activated ionic currents. The ATP concentration for half-maximal increase in [Ca2+]i was approximately 10 microM. Current activation and elevation of [Ca2+]i also occurred in Ca(2+)-free bath solutions but were abolished by loading the cells via the patch pipette with 10 mM 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid (BAPTA) or by preincubating the cells

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Arai, Takashi, Naoshi Takeyama, and Takaya Tanaka. "Glutathione monoethyl ester and inhibition of the oxyhemoglobin-induced increase in cytosolic calcium in cultured smooth-muscle cells." Journal of Neurosurgery 90, no. 3 (1999): 527–32. http://dx.doi.org/10.3171/jns.1999.90.3.0527.

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Object. The mechanism of arterial vasoconstriction caused by oxyhemoglobin production after subarachnoid hemorrhage was investigated.Methods. Using a fluorescent Ca++ indicator (fura-2 acetoxymethyl ester), the change in the cytosolic intracellular Ca++ concentration, [Ca++]i, was measured in cultured rat vascular smooth-muscle cells exposed to oxyhemoglobin and other substances. Oxyhemoglobin induced transient elevation of smooth-muscle cell [Ca++]i in either the presence or absence of ethyleneglycol-bis (β-aminoethylether)-N,N′-tetraacetic acid, indicating that Ca++ released by oxyhemoglobin

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Fan, Cheng, Xiaofang Yang, Wan Wendy Wang, et al. "Role of Kv1.3 Channels in Platelet Functions and Thrombus Formation." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 10 (2020): 2360–75. http://dx.doi.org/10.1161/atvbaha.120.314278.

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Objective: Platelet activation by stimulatory factors leads to an increase in intracellular calcium concentration ([Ca 2+ ] i ), which is essential for almost all platelet functions. Modulation of Ca 2+ influx and [Ca 2+ ] i in platelets has been emerging as a possible strategy for preventing and treating platelet-dependent thrombosis. Voltage-gated potassium 1.3 channels (Kv1.3) are highly expressed in platelets and able to regulate agonist-evoked [Ca 2+ ] i increase. However, the role of Kv1.3 channels in regulating platelet functions and thrombosis has not yet been elucidated. In addition,

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Kang, Sok Han, Pieter Vanden Berghe, and Terence K. Smith. "Ca2+-activated Cl− current in cultured myenteric neurons from murine proximal colon." American Journal of Physiology-Cell Physiology 284, no. 4 (2003): C839—C847. http://dx.doi.org/10.1152/ajpcell.00437.2002.

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Whole cell patch-clamp recordings were made from cultured myenteric neurons taken from murine proximal colon. The micropipette contained Cs+ to remove K+ currents. Depolarization elicited a slowly activating time-dependent outward current ( I tdo), whereas repolarization was followed by a slowly deactivating tail current ( I tail). I tdo and I tail were present in ∼70% of neurons. We identified these currents as Cl− currents ( I Cl), because changing the transmembrane Cl− gradient altered the measured reversal potential ( E rev) of both I tdo and I tail with that for I tailshifted close to the

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Salleo, A., G. La Spada, and R. Barbera. "Gadolinium is a powerful blocker of the activation of nematocytes of Pelagia noctiluca." Journal of Experimental Biology 187, no. 1 (1994): 201–6. http://dx.doi.org/10.1242/jeb.187.1.201.

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The activation properties of in situ nematocytes of Pelagia noctiluca (Scyphozoa) were investigated by physical contact with a gelatin probe that, besides stimulating the nematocyte battery, retains the discharged nematocysts, thereby allowing a quantitative evaluation of the response. In oral arms previously treated with 2 mmol l-1 La3+ the discharge was inhibited. This result confirms the Ca(2+)-dependence of nematocyte activation. A similar inhibitory effect was induced by treatment with 20 mumol l-1 Gd3+, a powerful blocker of mechanosensitive ion channels. It is therefore proposed that Ca

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Zhao, Y. J., J. Wang, L. J. Rubin, and X. J. Yuan. "Inhibition of K(V) and K(Ca) channels antagonizes NO-induced relaxation in pulmonary artery." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 2 (1997): H904—H912. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h904.

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Endogenous nitric oxide (NO) may contribute to the maintenance of normal pulmonary vasomotor tone, and inhaled NO is used to treat patients with pulmonary hypertension. Because pulmonary vascular tone is regulated by intracellular free Ca2+ concentration and membrane potential, which are controlled by the K+ channel activity in pulmonary artery (PA) smooth muscle cells, we sought to determine whether K+ channels are involved in NO-induced relaxation and, if so, which types of K+ channels are responsible. Authentic NO (approximately 0.3 microM) and sodium nitroprusside (SNP, 10 pM) both produce

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Schubert, R., V. N. Serebryakov, H. Mewes, and H. H. Hopp. "Iloprost dilates rat small arteries: role of K(ATP)- and K(Ca)-channel activation by cAMP-dependent protein kinase." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (1997): H1147—H1156. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1147.

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The effect of the stable prostacyclin analog iloprost and its mechanism of action were investigated with the use of pressurized rat tail small arteries with a spontaneous myogenic tone. Iloprost concentration dependently dilated these vessels with a half-maximal effective dose of 5.0 +/- 0.5 x 10(-8) M. Application of 10(-7)-10(-6) M glibenclamide, a blocker of ATP-sensitive potassium (K(ATP)) channels, inhibited the iloprost-induced dilation. Glibenclamide did not affect the basal vessel diameter. The application of 5 x 10(-5)-10(-3) M tetraethylammonium (TEA) and 5 x 10(-9)-10(-7) M iberioto

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Frindt, G., and L. G. Palmer. "Ca-activated K channels in apical membrane of mammalian CCT, and their role in K secretion." American Journal of Physiology-Renal Physiology 252, no. 3 (1987): F458—F467. http://dx.doi.org/10.1152/ajprenal.1987.252.3.f458.

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High conductance, Ca-activated K channels were studied in the apical membrane of the rat cortical collecting tubule (CCT) using the patch-clamp technique. In cell-attached patches the channels were found mainly in the closed state at the spontaneous apical membrane potential. They spent progressively more time in the open state as the pipette potential was made negative relative to the bath. In excised patches these channels had a high selectivity for K over Na and were activated by micromolar concentrations of Ca2+ on the cytoplasmic side of the membrane in a voltage-dependent manner. They ha

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Asano, M., K. Masuzawa-Ito, T. Matsuda, Y. Imaizumi, M. Watanabe, and K. Ito. "Functional role of Ca(2+)-activated K+ channels in resting state of carotid arteries from SHR." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 3 (1993): H843—H851. http://dx.doi.org/10.1152/ajpheart.1993.265.3.h843.

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Carotid arteries from spontaneously hypertensive rats (SHR) exhibited an active tone when exposed to a physiological salt solution; that is, the tension decreased when nifedipine was added. To determine the possible role of Ca(2+)-activated K+ (KCa) channels in the resting state of these arteries, the effects of agents that interact with these channels on tension and 86Rb efflux were compared in endothelium-denuded strips of carotid arteries from SHR and normotensive Wistar-Kyoto rats (WKY). The addition of charybdotoxin, a blocker of high-conductance KCa channels, to the resting strips produc

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Lin, C. S., R. C. Boltz, J. T. Blake, et al. "Voltage-gated potassium channels regulate calcium-dependent pathways involved in human T lymphocyte activation." Journal of Experimental Medicine 177, no. 3 (1993): 637–45. http://dx.doi.org/10.1084/jem.177.3.637.

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The role that potassium channels play in human T lymphocyte activation has been investigated by using specific potassium channel probes. Charybdotoxin (ChTX), a blocker of small conductance Ca(2+)-activated potassium channels (PK,Ca) and voltage-gated potassium channels (PK,V) that are present in human T cells, inhibits the activation of these cells. ChTX blocks T cell activation induced by signals (e.g., anti-CD2, anti-CD3, ionomycin) that elicit a rise in intracellular calcium ([Ca2+]i) by preventing the elevation of [Ca2+]i in a dose-dependent manner. However, ChTX has no effect on the acti

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Carrier, G. O., L. C. Fuchs, A. P. Winecoff, A. D. Giulumian, and R. E. White. "Nitrovasodilators relax mesenteric microvessels by cGMP-induced stimulation of Ca-activated K channels." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 1 (1997): H76—H84. http://dx.doi.org/10.1152/ajpheart.1997.273.1.h76.

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Nitric oxide (NO) released from endothelial cells or exogenous nitrates is a potent dilator of arterial smooth muscle; however, the molecular mechanisms mediating relaxation to NO in the microcirculation have not been characterized. The present study investigated the relaxant effect of nitrovasodilators on microvessels obtained from the rat mesentery and also employed whole cell and single-channel patch-clamp techniques to identify the molecular target of NO action in myocytes from these vessels. Both sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) relaxed phenylephrine-i

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Chen, Y., S. M. Simasko, J. Niggel, W. J. Sigurdson, and F. Sachs. "Ca2+ uptake in GH3 cells during hypotonic swelling: the sensory role of stretch-activated ion channels." American Journal of Physiology-Cell Physiology 270, no. 6 (1996): C1790—C1798. http://dx.doi.org/10.1152/ajpcell.1996.270.6.c1790.

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Hypotonic cell swelling triggers an increase in intracellular Ca2+ concentration that is deemed responsible for the subsequent regulated volume decrease in many cells. To understand the mechanisms underlying this increase, we have studied the Ca2+ sources that contribute to hypotonic cell swelling-induced Ca2+ increase (HICI) in GH3 cells. Fura 2 fluorescence of cell populations revealed that extracellular, but not intracellular, stores of Ca2+ were required. HICI was abolished by nifedipine, a blocker of L-type Ca2+ channels, and Gd3+, a nonspecific blocker of stretch-activated channels (SACs

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Kawanabe, Yoshifumi, Tomoh Masaki, and Nobuo Hashimoto. "Effects of the Ca++-permeable nonselective cation channel blocker LOE 908 on subarachnoid hemorrhage—induced vasospasm in the basilar artery in rabbits." Journal of Neurosurgery 98, no. 3 (2003): 561–64. http://dx.doi.org/10.3171/jns.2003.98.3.0561.

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Object. The Ca++ influx into vascular smooth-muscle cells (VSMCs) plays a fundamental role in the development and chronic effects of vasospasm after subarachnoid hemorrhage (SAH). The Ca++-permeable nonselective cation channels (NSCCs) are activated by several endothelium-derived constricting factors such as endothelin 1 (ET-1) and thromboxane A2. Moreover, the receptor-operated Ca++ channel blocker LOE 908 inhibits ET-1—induced extracellular Ca++ influx via NSCCs in the VSMCs of the basilar artery (BA) and the NSCC-dependent part of ET-1—induced vasoconstriction of BA rings. The purpose of th

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Vanelli, G., H. Y. Chang, A. G. Gatensby, and S. N. Hussain. "Contribution of potassium channels to active hyperemia of the canine diaphragm." Journal of Applied Physiology 76, no. 3 (1994): 1098–105. http://dx.doi.org/10.1152/jappl.1994.76.3.1098.

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Glibenclamide, iberiotoxin, and apamin (blockers of ATP-sensitive, large-conductance, and small-conductance Ca(2+)-activated K+ channels, respectively) were infused into the diaphragmatic vasculature of anesthetized indomethacin-treated dogs to assess the contribution of K+ channels to active hyperemia. Diaphragmatic blood flow (Qphr) and O2 uptake (VO2di) were measured at rest and during 2 min of continuous left phrenic nerve stimulation at 0.5, 1, 2, and 4 Hz. These measurements were repeated before (control) and after the infusion of a selective K+ channel blocker in three groups of animals

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