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Université Paris Descartes, Sorbonne Paris Cité, Paris, France
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Université Paris Descartes, Sorbonne Paris Cité, Paris, France
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Université Paris Descartes, Sorbonne Paris Cité, Paris, France
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Université Paris Descartes, Sorbonne Paris Cité, Paris, France
Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Service de Génétique, Paris, France
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pathogenic model for PA development. Recurrent somatic mutations were identified in genes coding for ion channels ( KCNJ5 Choi et al. 2011 and CACNA1D Azizan et al. 2013 , Scholl et al. 2013 ) and ATPases ( ATP1A1 and ATP2B3 , Azizan et al
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Nephrology and Hypertension Section, North Florida/South Georgia Veterans Health System, Gainesville, Florida, USA
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Rhesus C glycoprotein (Rhcg), an ammonia transporter, is a key molecule in urinary acid excretion and is expressed mainly in the intercalated cells (ICs) of the renal collecting duct. In the present study we investigated the role of aldosterone in the regulation of Rhcg expression. In in vivo experiments using C57BL/6J mice, Western blot analysis showed that continuous subcutaneous administration of aldosterone increased the expression of Rhcg in membrane fraction of the kidney. Supplementation of potassium inhibited the effect of aldosterone on the Rhcg. Next, mice were subjected to adrenalectomy with or without administration of aldosterone, and then ad libitum 0.14 M NH4Cl containing water was given. NH4Cl load increased the expression of Rhcg in membrane fraction. Adrenalectomy decreased NH4Cl-induced Rhcg expression, which was restored by administration of aldosterone. Immunohistochemical studies revealed that NH4Cl load induced the localization of Rhcg at the apical membrane of ICs in the outer medullary collecting duct. Adrenalectomy decreased NH4Cl-induced membrane localization of Rhcg, which was restored by administration of aldosterone. For in vitro experiments, IN-IC cells, an immortalized cell line stably expressing Flag-tagged Rhcg (Rhcg-Flag), were used. Western blot analysis showed that aldosterone increased the expression of Rhcg-Flag in membrane fraction, while the increase in extracellular potassium level inhibited the effect of aldosterone. Both spironolactone and Gӧ6983, a PKC inhibitor, inhibited the expression of Rhcg-Flag in the membrane fraction. These results suggest that aldosterone regulates the membrane expression of Rhcg through the mineralocorticoid receptor and PKC pathways, which is modulated by extracellular potassium level.
Division of Nephrology and Hypertension, Department of Physiology and Biophysics, Department of Medicine
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Cardiotonic steroids have been used for the past 200 years in the treatment of congestive heart failure. As specific inhibitors of membrane-bound Na+/K+ ATPase, they enhance cardiac contractility through increasing myocardial cell calcium concentration in response to the resulting increase in intracellular Na concentration. The half-minimal concentrations of cardiotonic steroids required to inhibit Na+/K+ ATPase range from nanomolar to micromolar concentrations. In contrast, the circulating levels of cardiotonic steroids under physiological conditions are in the low picomolar concentration range in healthy subjects, increasing to high picomolar levels under pathophysiological conditions including chronic kidney disease and heart failure. Little is known about the physiological function of low picomolar concentrations of cardiotonic steroids. Recent studies have indicated that physiological concentrations of cardiotonic steroids acutely stimulate the activity of Na+/K+ ATPase and activate an intracellular signaling pathway that regulates a variety of intracellular functions including cell growth and hypertrophy. The effects of circulating cardiotonic steroids on renal salt handling and total body sodium homeostasis are unknown. This review will focus on the role of low picomolar concentrations of cardiotonic steroids in renal Na+/K+ ATPase activity, cell signaling, and blood pressure regulation.
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Introduction: response to osmotic stimuli – a function of TRPV ion channels, apparent since ‘birth’ of this subfamily Within the transient receptor potential (TRP) superfamily of ion channels ( Cosens & Manning 1969 , Montell
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colour version of this figure available via http://dx.doi.org/10.1530/JOE-10-0431 . Altered expression of Ca 2 + cycling/ion channel genes in DEX-induced hypertrophied heart To examine the effect of GC treatment on cardiac gene expression
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can also contribute to the direct regulation of some ion channels ( Hardie 2003 ). This elegantly simple concept marked only the beginning of an amazing explosion of research into phosphoinositides, and almost every component of the calcium
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Division of Endocrinology and Diabetology, Department of Neurosurgery, Division of Endocrinology and Diabetology, Department of Neurosurgery, University Hospital Zurich, Rämistrasse 100, CH-8091 Zurich, Switzerland
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Division of Endocrinology and Diabetology, Department of Neurosurgery, Division of Endocrinology and Diabetology, Department of Neurosurgery, University Hospital Zurich, Rämistrasse 100, CH-8091 Zurich, Switzerland
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al . 2008 ), and the regulation of plasma membrane amount and activity of ion channels and transporters, e.g. to attenuate calciuria. There is an ongoing debate on whether FGF23 can exert physiologically relevant effects on cells that do not express
INSERM, University Paris Descartes, Assistance Publique-Hôpitaux de Paris, UMRS_970, Paris Cardiovascular Research Center – PARCC, 56, rue Leblanc, 75015 Paris, France
INSERM, University Paris Descartes, Assistance Publique-Hôpitaux de Paris, UMRS_970, Paris Cardiovascular Research Center – PARCC, 56, rue Leblanc, 75015 Paris, France
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INSERM, University Paris Descartes, Assistance Publique-Hôpitaux de Paris, UMRS_970, Paris Cardiovascular Research Center – PARCC, 56, rue Leblanc, 75015 Paris, France
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INSERM, University Paris Descartes, Assistance Publique-Hôpitaux de Paris, UMRS_970, Paris Cardiovascular Research Center – PARCC, 56, rue Leblanc, 75015 Paris, France
INSERM, University Paris Descartes, Assistance Publique-Hôpitaux de Paris, UMRS_970, Paris Cardiovascular Research Center – PARCC, 56, rue Leblanc, 75015 Paris, France
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and DNA extracted from APA (somatic DNA). Recurrent somatic mutations in genes coding for ion channels ( KCNJ5 ( Choi et al . 2011 ) and CACNA1D ( Azizan et al . 2013 , Scholl et al . 2013 )) and ATPases ( ATP1A1 and ATP2B3 ( Beuschlein et
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-cells: from ion channel activity to exocytosis Pancreatic α-cells are equipped with a specific set of channels that generate action potentials of Na + and Ca 2 + in the absence or at low levels of glucose ( Gromada et al . 1997 ). This electrical activity
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ABSTRACT
Cultured porcine thyroid cells exhibit a resting membrane potential of about − 73 mV and depolarize to about − 54 mV on exposure to TSH. The depolarizing response to TSH was preserved in a medium consisting only of inorganic salts and buffers, but was abolished in sodium-free medium, demonstrating dependence on an inward sodium current. Increasing the potassium concentration of the medium resulted in a reduction in the resting membrane potential of 60 mV per tenfold change in potassium concentration, and a diminished TSH response. A hyperpolarizing TSH response was observed in a sodium- and bicarbonate-free medium, indicating that a hyperpolarizing ion current (probably carried by potassium) was also enhanced in the presence of TSH. Tetrodotoxin blocked the TSH response. We conclude that the response of the thyroid cell membrane to TSH involves increases in permeability to sodium and potassium, and that the thyroid membrane ion channels bear some similarity to the voltage-dependent sodium channels of excitable tissues, despite the absence of action potentials in the thyroid.
J. Endocr. (1986) 108, 225–230
