Participation of Ca2+ channel in liver calcium regulation by calcitonin in rats

Abstract. A possible regulatory role of calcitonin (CT) upon liver calcium content was investigated by using a Ca2+ channel blocker in thyroparathyroidectomized (TPTX) rats. In bile duct-ligated TPTX rats, liver calcium content was not significantly increased by a single ip injection of calcium chloride (4.0 mg Ca2+/100 g body weight). Administration of CT (80 MRC mU/100 g) caused a remarkable elevation of liver calcium content. This hormonal effect was inhibited by administration of verapamil (1.0 mg/100 g) or lanthanum chloride (0.4 mg/100 g), Ca2+ channel blockers. CT administration markedly increased the transport of calcium into the bile through the liver cells of TPTX rats injected ip with calcium. This increase in the bile calcium content was prevented by administration of verapamil or lanthanum chloride. Administration of epinephrine (10 μg/100 g), vasopressin (10 μg/100 g), or concanavalin A (1.0 mg/100 g) produced a significant elevation of bile calcium content; these elevations were not significantly altered by addition of verapamil (1.0 mg/100 g). These data suggest the presence of CT receptors on liver cell plasma membranes which are involved in regulation of membrane Ca2+ channels. It is proposed that CT facilitates the entry of extracellular calcium into liver cells by opening Ca2+ channels located on their plasma membranes.

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Role of K+ channels in adrenal catecholamine secretion in anesthetized dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.4.r1125 ◽

1998 ◽

Vol 274 (4) ◽

pp. R1125-R1130 ◽

Cited By ~ 2

Author(s):

Takahiro Nagayama ◽

Kimiya Masada ◽

Makoto Yoshida ◽

Mizue Suzuki-Kusaba ◽

Hiroaki Hisa ◽

...

Keyword(s):

Channel Blocker ◽

Splanchnic Nerve ◽

Channel Blockers ◽

Cholinergic Agonists ◽

Voltage Dependent ◽

Anesthetized Dogs ◽

Splanchnic Nerve Stimulation ◽

Mast Cell Degranulating ◽

Small Conductance

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 (0.1–0.4 μg), or muscarine (0.5–2 μg). The small-conductance Ca2+-activated K+(SKCa) channel blocker scyllatoxin infusion (10–100 ng/min) enhanced the ACh-, DMPP-, and muscarine-induced increases in CA output, but it did not affect the SNS-induced increases in CA output. These results suggest that KA channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SKCa channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.

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Polyphenols as Modulators of Aquaporin Family in Health and Disease

Oxidative Medicine and Cellular Longevity ◽

10.1155/2015/196914 ◽

2015 ◽

Vol 2015 ◽

pp. 1-8 ◽

Cited By ~ 20

Author(s):

Diana Fiorentini ◽

Laura Zambonin ◽

Francesco Vieceli Dalla Sega ◽

Silvana Hrelia

Keyword(s):

Plasma Membranes ◽

Skin Diseases ◽

Water Channel ◽

Bioactive Molecules ◽

Food Sources ◽

Major Function ◽

Cell Plasma ◽

Original Analysis ◽

Health And Disease

Polyphenols are bioactive molecules widely distributed in fruits, vegetables, cereals, and beverages. Polyphenols in food sources are extensively studied for their role in the maintenance of human health and in the protection against development of chronic/degenerative diseases. Polyphenols act mainly as antioxidant molecules, protecting cell constituents against oxidative damage. The enormous number of polyphenolic compounds leads to huge different mechanisms of action not fully understood. Recently, some evidence is emerging about the role of polyphenols, such as curcumin, pinocembrin, resveratrol, and quercetin, in modulating the activity of some aquaporin (AQP) isoforms. AQPs are integral, small hydrophobic water channel proteins, extensively expressed in many organs and tissues, whose major function is to facilitate the transport of water or glycerol over cell plasma membranes. Here we summarize AQP physiological functions and report emerging evidence on the implication of these proteins in a number of pathophysiological processes. In particular, this review offers an overview about the role of AQPs in brain, eye, skin diseases, and metabolic syndrome, focusing on the ability of polyphenols to modulate AQP expression. This original analysis can contribute to elucidating some peculiar effects exerted by polyphenols and can lead to the development of an innovative potential preventive/therapeutic strategy.

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Characterization of the binding of diadenosine 5′,5‴-P1,P4-tetraphosphate (Ap4A) to rat liver cell membranes

Biochemical Journal ◽

10.1042/bj3140687 ◽

1996 ◽

Vol 314 (2) ◽

pp. 687-693 ◽

Cited By ~ 17

Author(s):

Mandy EDGECOMBE ◽

Alexander G. McLENNAN ◽

Michael J. FISHER

Keyword(s):

Plasma Membrane ◽

Rat Liver ◽

Liver Cell ◽

Plasma Membranes ◽

Rank Order ◽

Liver Cells ◽

Diadenosine Polyphosphates ◽

Cell Plasma ◽

Isolated Liver Cells ◽

Isolated Liver

Diadenosine polyphosphates present in the extracellular environment can, through interaction with appropriate purinoceptors, influence a range of cellular activities. Here we have investigated the nature of the ligand:receptor interactions involved in diadenosine 5′,5″-P1,P4-tetraphosphate (Ap4A)-mediated stimulation of glycogen breakdown in isolated rat liver cells. [2-3H]Ap4A showed specific binding to both intact isolated liver cells and plasma membrane fractions prepared from isolated liver cells. HPLC analysis confirmed that binding was mediated by intact Ap4A and not by potential breakdown products (e.g. ATP, adenosine etc). Binding of [2-3H]Ap4A, to isolated liver cell plasma membrane preparations, was successfully displaced by a range of both naturally occurring and synthetic diadenosine polyphosphates with the rank order potency Ap4A ⩾Ap5A > Ap6A > Ap3A > Ap2A. [2-3H]Ap4A binding was not displaced by P1 effectors but was successfully displaced by a range of P2 effectors with the rank order potency 2-methylthio-ATP > ATP > ADP ⩾adenosine 5′-[αβ-methylene]triphosphate > adenosine 5′-[βγ-methylene]triphosphate. These findings are consistent with the interaction of Ap4A with a P2y-like subclass of purinoceptor and are discussed in relation to (1) the known purinoceptor populations in liver cell plasma membranes and (2) observations concerning the binding of diadenosine polyphosphates to purinoceptors in other tissues.

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N-Type Voltage-Dependent Calcium Channels Mediate the Nicotinic Enhancement of GABA Release in Chick Brain

Journal of Neurophysiology ◽

10.1152/jn.1999.81.2.447 ◽

1999 ◽

Vol 81 (2) ◽

pp. 447-454 ◽

Cited By ~ 24

Author(s):

Trevor L. Tredway ◽

Jian-Zhong Guo ◽

Vincent A. Chiappinelli

Keyword(s):

Calcium Channels ◽

Channel Blocker ◽

Brain Slices ◽

Gaba Release ◽

Channel Blockers ◽

Chick Brain ◽

Voltage Dependent ◽

Voltage Dependent Calcium Channels ◽

Whole Cell Recordings

N-type voltage-dependent calcium channels mediate the nicotinic enhancement of GABA release in chick brain. The role of voltage-dependent calcium channels (VDCCs) in the nicotinic acetylcholine receptor (nAChR)-mediated enhancement of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) was investigated in chick brain slices. Whole cell recordings of neurons in the lateral spiriform (SpL) and ventral lateral geniculate (LGNv) nuclei showed that cadmium chloride (CdCl2) blocked the carbachol-induced increase of spontaneous GABAergic IPSCs, indicating that VDCCs might be involved. To conclusively show a role for VDCCs, the presynaptic effect of carbachol on SpL and LGNv neurons was examined in the presence of selective blockers of VDCC subtypes. ω-Conotoxin GVIA, a selective antagonist of N-type channels, significantly reduced the nAChR-mediated enhancement of γ-aminobutyric acid (GABA) release in the SpL by 78% compared with control responses. Nifedipine, an L-type channel blocker, and ω-Agatoxin-TK, a P/Q-type channel blocker, did not inhibit the enhancement of GABAergic IPSCs. In the LGNv, ω-Conotoxin GVIA also significantly reduced the nAChR-mediated enhancement of GABA release by 71% from control values. Although ω-Agatoxin-TK did not block the nicotinic enhancement, L-type channel blockers showed complex effects on the nAChR-mediated enhancement. These results indicate that the nAChR-mediated enhancement of spontaneous GABAergic IPSCs requires activation of N-type channels in both the SpL and LGNv.

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Role of calcium channel blocker in excessive mast cell degranulation

International Journal of Medical and Biomedical Studies ◽

10.32553/ijmbs.v5i7.1981 ◽

2021 ◽

Vol 5 (7) ◽

Author(s):

Sagarika Datta

Keyword(s):

Mast Cell ◽

Peripheral Neuropathy ◽

Anxiety Disorder ◽

Calcium Channel ◽

Female Patient ◽

Calcium Channel Blockers ◽

Channel Blocker ◽

Mast Cell Degranulation ◽

Channel Blockers

Here, I present a case of a female patient, age 45 years, for whom the uncontrolled mast cell degranulation created many issues related to allergy like, skin rash, itching, breathing discomfort, frequent throat infection, GERD, migraine, fibromyalgia, peripheral neuropathy, depression, anxiety disorder, constipation etc. For the patient, it was observed that calcium channel blockers seem to control the unnecessary and uncontrolled mast cell degranulation. CCB seemed to have a role to play in mast cell degranulation.

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Significance of the calcium content of mouse β cells in the preservation of glucose-induced insulin release during culture

Journal of Endocrinology ◽

10.1677/joe.0.1150027 ◽

1987 ◽

Vol 115 (1) ◽

pp. 27-34 ◽

Cited By ~ 1

Author(s):

P. Bergsten

Keyword(s):

Insulin Release ◽

Channel Blocker ◽

Calcium Content ◽

Secretory Response ◽

Immunoreactive Insulin ◽

Β Cells ◽

Intracellular Ca ◽

Insulin Secretory Response ◽

Established Role

ABSTRACT Pancreatic islets containing more than 90% β cells from obese–hyperglycaemic (ob/ob) mice were cultured for 3 days in different concentrations of Ca2+ and glucose to evaluate the importance of intracellular Ca2+ sequestration in glucose-induced insulin release. The islet contents of calcium (total and exchangeable) and immunoreactive insulin were compared with the insulin secretory response to glucose after culture. The turnover of Ca2+ increased with increasing concentrations of glucose and Ca2+. Islets cultured in the presence of 5.5 mmol glucose/1 contained more calcium and insulin than those cultured with 1 or 20 mmol glucose/1. During culture in 20 mmol glucose/1, a lowering of the Ca2+ concentration of the medium from 0.42 to 0.025 mmol/l resulted in a paradoxical increase in intracellular calcium, with improvement of the subsequent secretory response to the sugar. When the islets had been exposed to the calcium channel blocker D-600 during culture in a Ca2+-deficient medium, substantial insulin release was noted from islets containing relatively small amounts of calcium. The results suggest that the well-established role of glucose in maintaining insulin release is associated with an ability of the sugar to stimulate the retention of calcium in β cells. J. Endocr. (1987) 115, 27-34

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Cross-Talk between Lipoproteins and Inflammation: The Role of Microvesicles

Journal of Clinical Medicine ◽

10.3390/jcm8122059 ◽

2019 ◽

Vol 8 (12) ◽

pp. 2059 ◽

Cited By ~ 1

Author(s):

Gemma Chiva-Blanch ◽

Lina Badimon

Keyword(s):

Plasma Membranes ◽

Oxidized Ldl ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Plaque Vulnerability ◽

Therapeutic Approaches ◽

Common Features ◽

Cell Plasma ◽

Novel Therapeutic

Atherothrombosis is the principal underlying cause of cardiovascular disease (CVD). Microvesicles (MV) are small blebs originated by an outward budding at the cell plasma membranes, which are released in normal conditions. However, MV release is increased in pathophysiologic conditions such as CVD. Low density lipoprotein (LDL) and MV contribute to atherothrombosis onset and progression by promoting inflammation and leukocyte recruitment to injured endothelium, as well as by increasing thrombosis and plaque vulnerability. Moreover, (oxidized)LDL induces MV release and vice-versa, perpetuating endothelium injury leading to CVD progression. Therefore, MV and lipoproteins exhibit common features, which should be considered in the interpretation of their respective roles in the pathophysiology of CVD. Understanding the pathways implicated in this process will aid in developing novel therapeutic approaches against atherothrombosis.

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Global genetic deletion of CaV3.3 channels facilitates anaesthetic induction and enhances isoflurane-sparing effects of T-type calcium channel blockers

Scientific Reports ◽

10.1038/s41598-020-78488-8 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Simon Feseha ◽

Tamara Timic Stamenic ◽

Damon Wallace ◽

Caesare Tamag ◽

Lingling Yang ◽

...

Keyword(s):

Channel Blocker ◽

Mutant Mice ◽

Channel Blockers ◽

Volatile Anaesthetics ◽

Wild Type ◽

Anaesthetic Induction ◽

Knock Out ◽

Valuable Adjunct ◽

Genetic Deletion

AbstractWe previously documented that the CaV3.3 isoform of T-type calcium channels (T-channels) is inhibited by clinically relevant concentrations of volatile anaesthetics, including isoflurane. However, little is understood about the functional role of CaV3.3 channels in anaesthetic-induced hypnosis and underlying neuronal oscillations. To address this issue, we used CaV3.3 knock-out (KO) mice and a panselective T-channel blocker 3,5-dichloro-N-[1-(2,2-dimethyltetrahydro-pyran-4-ylmethyl)-4-fluoro-piperidin-4-ylmethyl]-benzamide (TTA-P2). We found that mutant mice injected with the vehicle showed faster induction of hypnosis than wild-type (WT) mice, while the percent isoflurane at which hypnosis and immobility occurred was not different between two genotypes. Furthermore, we found that TTA-P2 facilitated isoflurane induction of hypnosis in the CaV3.3 KO mice more robustly than in the WT mice. Isoflurane-induced hypnosis following injections of TTA-P2 was accompanied with more prominent delta and theta EEG oscillations in the mutant mice, and reached burst-suppression pattern earlier when compared to the WT mice. Our findings point to a relatively specific value of CaV3.3 channels in anaesthetic induced hypnosis. Furthermore, we propose that T-channel blockers may be further explored as a valuable adjunct to reducing the usage of potent volatile anaesthetics, thereby improving their safety.

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The vaso-contractile action of zooxanthellatoxin-B from a marine dinoflagellate is mediated via Ca2+ influx in the rabbit aorta

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y01-089 ◽

2001 ◽

Vol 79 (12) ◽

pp. 1030-1035 ◽

Cited By ~ 1

Author(s):

Takahiro Moriya ◽

Ken-Ichi Furukawa ◽

Hideshi Nakamura ◽

Akio Murai ◽

Yasushi Ohizumi

Keyword(s):

Channel Blocker ◽

Rabbit Aorta ◽

Simultaneous Recording ◽

Channel Blockers ◽

Dependent Manner ◽

Free Solution ◽

Half Maximum ◽

Concentration Dependent Manner ◽

Time Required

We previously showed that zooxanthellatoxin-B, isolated from dinoflagellate, caused a sustained contraction of the aorta in an external Ca2+-dependent manner. To clarify the role of Ca2+ in this action, we examined the effects of zooxanthellatoxin-B as well as a depolarizing stimulus (60 mM KCl), using the simultaneous recording for cytosolic Ca2+ level (fura-2) and developed tension in the rabbit aorta. KCl (60 mM) elicited a rapid cytosolic Ca2+ elevation followed by a pronounced contraction, and time required for half-maximum contraction was 2 min. Zooxanthellatoxin-B caused an increase in cytosolic Ca2+ followed by a gradual contraction, with a time for half-maximum contraction of 510 min in a concentration-dependent manner. We found a strong correlation between Ca2+ elevation and the contraction in zooxanthellatoxin-B action. In a Ca2+-free solution, zooxanthellatoxin-B caused neither the contraction nor the increase in cytosolic Ca2+. Furthermore, both pre- and post-treatment with verapamil, a voltage-operated Ca2+-channel blocker, partially suppressed both an increase in cytosolic Ca2+ and the contraction by zooxanthellatoxin-B. Zooxanthellatoxin-B-induced contraction was also inhibited by other voltage-operated Ca2+-channel blockers: nifedipine or diltiazem. These results suggest that zooxanthellatoxin-B-elicited contraction is caused by a Ca2+ influx into the smooth muscle cells, partially via voltage-operated Ca2+ channels.Key words: zooxanthellatoxin, Ca2+ imaging, rabbit aorta, contraction, voltage-operated Ca2+-channels.

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