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Tingting Yang, Min He, Hailiang Zhang, Paula Q Barrett and Changlong Hu

PA ( Funder et al . 2008 , Monticone et al . 2017 ). Notably, somatic mutations of potassium and calcium channels have been found in more than half of aldosterone-producing adenomas ( Yang et al . 2018 ). Intracellular Ca 2+ regulates key steps

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Hongyu Su, Xueyi Chen, Yueming Zhang, Linglu Qi, Yun He, Juanxiu Lv, Yingying Zhang, Xiang Li, Jiaqi Tang and Zhice Xu

, while AT2R may mediate vasodilation ( Tang et al. 2017 ). Following combining with its G protein-coupled receptors, a series of calcium channels and calcium-sensitive signaling pathway are triggered to regulate vascular tone. L-type voltage

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A M Davalli, E Biancardi, A Pollo, C Socci, A E Pontiroli, G Pozza, F Clementi, E Sher and E Carbone


Calcium ion entry through voltage-operated calcium channels is a crucial step in the coupling of β cell depolarization with insulin secretion. Various calcium channel subtypes have been shown to be coexpressed in single neurons and endocrine cells. Using the patch-clamp technique, we investigated the biophysical and pharmacological properties of calcium channels in freshly dispersed human pancreatic β cells.

Both low and high voltage activated currents were expressed, the two current types being easily distinguishable on the basis of biophysical criteria. The high voltage activated currents were not homogeneous: one component was affected by the dihydropyridine antagonist nitrendipine and the agonist Bay-K-8644; the other was insensitive to both dihydropyridines and ω-conotoxin GVIA. In line with this pharmacology, nitrendipine reduced and Bay-K-8644 increased glucose-induced insulin secretion from perifused human islets, whereas ω-conotoxin GVIA had no effect. However, about 20% of the glucose-induced insulin release was found to be resistant to high nitrendipine concentrations.

These data show that human pancreatic β cells express heterogeneous voltage-operated calcium channels, only one of which is dihydropyridine-sensitive (L type). The L type channels are clearly involved in the control of insulin secretion, but our data suggest that dihydropyridine- and ω-conotoxin GVIA-insensitive channels may also play a role in the stimulus-secretion coupling of human β cells.

Journal of Endocrinology (1996) 150, 195–203

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RD Jones, LN Ruban, IE Morton, SA Roberts, KM English, KS Channer and TH Jones

Testosterone-induced vasodilatation is proposed to contribute to the beneficial effects associated with testosterone replacement therapy in men with cardiovascular disease, and is postulated to occur via either direct calcium channel blockade, or through potassium channel activation via increased production of cyclic nucleotides. We utilised flow cytometry to investigate whether testosterone inhibits the increase in cellular fluorescence induced by prostaglandin F(2alpha) in A7r5 smooth muscle cells loaded with the calcium fluorescent probe indo-1-AM, and to study the cellular mechanisms involved. Two-minute incubation with testosterone (1 microM) significantly inhibited the change in cellular fluorescence in response to prostaglandin F(2alpha) (10 microM) (3.6+/-0.6 vs 7.6+/-1.0 arbitrary units, P=0.001). The change in cellular fluorescence in response to prostaglandin F(2alpha) (10 microM) was also significantly attenuated in the absence of extracellular calcium (3.6+/-0.3 vs 15.6+/-0.7 arbitrary units, P=0.0000002), and by a 2-min incubation with the store-operated calcium channel blocker SK&F 96365 (50 microM) (4.7+/-0.8 vs 8.1+/-0.4 arbitrary units, P=0.003). The response was insensitive to similar incubation with the voltage-operated calcium channel blockers verapamil (10 microM) (12.6+/-1.2 vs 11.9+/-0.2 arbitrary units, P=0.7) or nifedipine (10 microM) (13.9+/-1.3 vs 13.3+/-0.5 arbitrary units, P=0.7). Forskolin (1 microM) and sodium nitroprusside (100 microM) significantly increased the cellular concentration of cyclic adenosine monophosphate and cyclic guanosine monophosphate respectively, but testosterone (100 nM-100 microM) had no effect. These data indicate that the increase in intracellular calcium in response to prostaglandin F(2alpha) occurs primarily via extracellular calcium entry through store-operated calcium channels. Testosterone inhibits the response, suggesting an antagonistic action upon these channels.

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Akhilesh K Pandey, Wei Li, Xiangling Yin, Douglas M Stocco, Paula Grammas and XingJia Wang

testosterone production in mouse Leydig cells . Journal of Andrology 12 148 – 151 . Moger WH 1983 Effects of the calcium-channel blockers cobalt, verapamil, and D600 on Leydig cell steroidogenesis . Biology of Reproduction 28 528 – 535 . Payne

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Olena A Fedorenko, Pawitra Pulbutr, Elin Banke, Nneoma E Akaniro-Ejim, Donna C Bentley, Charlotta S Olofsson, Sue Chan and Paul A Smith

blocking buffer (PBS with 3% BSA and 0.5% Triton-100x) for 10 min then stained with primary anti-Calcium Channel L-type alpha 1C subunit (Cacna1C) antibody conjugated with Atto 594 (ACC-003-AG, Alomone) at 1:200 dilution for 16 h ( Raifman et al. 2017

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K Stelwagen and MR Callaghan

Tight junctions (TJs) play an essential role in cell-cell contact between mammary epithelial cells and, as such, play a critical role in cell function. Moreover, calcium (Ca) plays a crucial role in the formation and maintenance of mammary TJs. Given that parathyroid hormone-related peptide (PTHrP) is involved in cellular Ca homeostasis, we postulated a role for PTHrP in the regulation of mammary TJs. The effect of PTHrP(1-34) on TJs was studied in the mouse mammary cell line COMMA-1D by measuring transepithelial electrical resistance across cell monolayers and measuring the expression of TJ proteins. PTHrP stimulated TJ formation but only under conditions where extracellular Ca was limiting. This effect of PTHrP appeared to be indirect and mediated via increased intracellular availability of Ca as a result of increased Ca-channel activity in the apical membrane. The changes in TJs were associated with altered expression of the TJ protein occludin, but expression of the TJ protein claudin-1 was not affected. The effects of PTHrP on mammary TJs are independent of prolactin. In conclusion, PTHrP enhances mammary TJ formation when extracellular Ca is limiting by maintaining intracellular Ca supplies.

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Manami Oya, Tetsuya Kitaguchi, Kazuki Harada, Rika Numano, Takahiro Sato, Masayasu Kojima and Takashi Tsuboi

Roenfeldt M Ammon HP Froschmayr M Cassidy TN Morano I Ahlijanian MK 1997 L-type calcium channels in insulin-secreting cells: biochemical characterization and phosphorylation in RINm5F cells . Molecular Endocrinology 11 619 – 629

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S. Batra


Ovariectomized rabbits were treated for 1 or 8 weeks with oestrogen and the effects on uterine weight, muscarinic receptor density and nitrendipine-binding sites on myometrial membranes were studied. The wet weight of the uterus after 1 week of oestrogen treatment increased more than tenfold and increased further by approximately 50% after 8 weeks of oestrogen treatment. The muscarinic receptor density increased significantly after 1 week of oestrogen treatment. Although there was no further increase in receptor density with continuing oestrogen treatment up to 8 weeks, the muscarinic receptor affinity increased significantly. The density of nitrendipine-binding sites increased sixfold after 1 week of oestrogen treatment and did not change thereafter. Oestrogen treatment had no influence on the affinity of nitrendipine-binding sites. The increase by oestrogen in muscarinic receptor density and in nitrendipine-binding sites as shown by the present data is consistent with the generally reported increase in agonist-induced contractile response of the myometrium following oestrogen treatment.

Journal of Endocrinology (1990) 125, 185–189

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Priyanka De, Sreerupa Ghose Roy, Dipak Kar and Arun Bandyopadhyay