Genome-independent effects of 1,25-dihydroxy vitamin D-3 on membrane potential

Edelman, A.; Thil, C. L.; Garabédian, M; Anagnostopoulos, T.; Balsan, S

doi:10.1016/0005-2736(83)90215-8

Cited by 15 publications

(8 citation statements)

References 11 publications

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“…Since these early responses to steroids clearly cannot be ascribed to de novo protein synthesis, they most likely reflect direct effect(s) on the cell membrane, e.g. changes of its ionic conductances [14]. This effect is consistent with the view that vitamin D metabolites, by virtue of their cholesterol-like configuration, are rapidly incorporated into the membrane leaflet, thus altering its physical properties [27].…”

Section: Introductionmentioning

confidence: 58%

“…[12][13][14]. Using perfusing pipettes having a tip diameter of 10 to 15/xm and applying high perfusion rates (-1 /zl/min), we empirically defined the minimal tip diameter of the collecting pipette ensuring nondistension of the tubule as 40/xm.…”

Section: Methodsmentioning

confidence: 99%

“…The methods for anesthesia, dissection of the animals and preparation of the kidney have been described elsewhere [1,2,[11][12][13][14].…”

Section: Methodsmentioning

confidence: 99%

“…We have also reported that vitamin D metabolites, 1,25(OH)2D3 and 25(OH)D3 (but not cholesterol), alter cell membrane potential of presumptive target cells, e.g. epiphyseal cartilage and renal proximal tubule cells but not myocytes, with a time course of the order of seconds [14,15]. Since these early responses to steroids clearly cannot be ascribed to de novo protein synthesis, they most likely reflect direct effect(s) on the cell membrane, e.g.…”

Section: Introductionmentioning

confidence: 93%

“…Since vitamin D metabolite-induced (rapid) changes of cell membrane potential may underlie some yet undefined physiologic action, the present work was undertaken to further characterize the ionic mechanisms associated with these changes. The experiments were performed in the proximal tubule of the amphibian Necturus maculosus, a preparation extensively investigated in this laboratory [1][2][3][4][11][12][13][14] and shown to be sensitive to vitamin D metabolites [14]. A large number of steroids and secosteroids 1 was tested in the present study to determine which molecules are effective in changing cell membrane potential and to attempt structure/function correlations.…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms of 1,25(OH)2D3-induced rapid changes of membrane potential in proximal tubule: Role of Ca2+-dependent K+ channels

1986

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Eleven different secosteroids or steroids (10(-10) to 10(-8) M) were acutely and reversibly introduced in solutions delivered to the lumen of single proximal tubules of the amphibian Necturus kidney while recording basolateral cell membrane potential Vm. Seven of these molecules (1,25(OH)2D3, 25(OH)D3, 24,25(OH)2D3, 5,6-trans-25(OH)D3, 19-diol-cholesterol, estradiol and testosterone) resulted in changes of Vm (delta Vm) occurring in a few seconds, the largest delta Vm being observed with 1,25(OH)2D3, +6.5 +/- 0.75 mV (n = 19); these seven (seco)steroids, but not the four inactive sterols (vitamin D3, cholesterol, 1 alpha D3 and aldosterone) possess a hydroxyl group on at least one carbon of the C17 to C25 lateral chain of the sterol ring. The delta Vm effect was present in Na+-free or Cl-free media, but it was abolished in HCO3-free media. Depolarization of cell membrane potential by addition of glucose, 11 mM, in luminal perfusion fluid abolished the 1,25(OH)2D3-evoked delta Vm effect, suggesting dependence of the latter on the absolute value of membrane potential. Barium, a blocking agent of K+ conductances, suppressed the 1,25(OH)2D3-evoked delta Vm effect, even when the proper effects of barium of cell membrane potential were canceled by current clamp. Pretreatment with quinine, a putative blocker of Ca2+-dependent K+ channels also abolished the 1,25(OH)2D3-evoked depolarization. Such observations are consistent with the presence of Ca2+-dependent K+ channels at the apical cell membrane of the proximal tubule, these channels being inactivated by 1,25(OH)2D3 and probably by other (seco)steroids.

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Section: Introductionmentioning

confidence: 58%

Section: Methodsmentioning

confidence: 99%

“…The methods for anesthesia, dissection of the animals and preparation of the kidney have been described elsewhere [1,2,[11][12][13][14].…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Mechanisms of 1,25(OH)2D3-induced rapid changes of membrane potential in proximal tubule: Role of Ca2+-dependent K+ channels

1986

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Oscillations in inositol 1,4,5-trisphosphate and diacyglycerol induced by vitamin D3 metabolites in confluent mouse osteoblasts

Grosse

Bourdeau

Lieberherr

1993

Journal of Bone and Mineral Research

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For the last 5 years, attention has focused on the nongenomic effects of 1,25-(OH)2D3, but considerably less is known about the mechanisms of the nonnuclear actions of 24,25-(OH)2D3. The present study examines and compares the rapid (5-90 s) effects of 100 pM to 10 nM 24,25-(OH)2D3, 10 pM to 1 nM 1,25-(OH)2D3, and 1-100 nM 25-OHD3 on the formation of inositol phosphates and lipids in confluent mouse osteoblasts. 24,25-(OH)2D3 and 25-OHD3 effects were dose dependent; those of 1,25-(OH)2D3 were dose dependent in a bell-shaped manner. The two dihydroxylated metabolites induced a multiphasic response in inositol 1,4,5-trisphosphate (IP3) formation with three stimulation peaks; the IP3 response to 25-OHD3 was monophasic. The amplitude of the IP3 response to 24,25-(OH)2D3 was greater and its oscillation period was slower than that induced by 1,25-(OH)2D3. The diacylglycerol (DAG) responses to secosteroids showed two stimulation peaks that appeared at different times depending on the secosteroid used. Pretreatment with neomycin totally inhibited the first DAG response; neomycin had no effect on the second peak of DAG induced by 25-OHD3, whereas it partially blocked the second response of DAG to 24,25-(OH)2D3 and 1,25-(OH)2D3. These data show for the first time that 24,25-(OH)2D3 can modulate phospholipid metabolism in confluent mouse osteoblasts as early as 5-10 s. The first pathway used by all three secosteroids is that of the hydrolysis of phosphatidylinositol 4,5-bisphosphate via phospholipase C activation, leading to the formation of the two second messengers, IP3 and DAG, since neomycin totally blocked the response. Thus, the action of these secosteroids on the osteoblast membrane may also implicate several steps of the phosphatidylcholine cycle, according to the metabolite tested. Finally, these data point to a direct interaction of vitamin D metabolites with specific membrane recognition moieties.

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The Neuromuscular Manifestations of Primary Hyperparathyroidism in Humans

Yamaguchi

1989

New Actions of Parathyroid Hormone

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Genome-independent effects of 1,25-dihydroxy vitamin D-3 on membrane potential

Cited by 15 publications

References 11 publications

Mechanisms of 1,25(OH)2D3-induced rapid changes of membrane potential in proximal tubule: Role of Ca2+-dependent K+ channels

Mechanisms of 1,25(OH)2D3-induced rapid changes of membrane potential in proximal tubule: Role of Ca2+-dependent K+ channels

Oscillations in inositol 1,4,5-trisphosphate and diacyglycerol induced by vitamin D3 metabolites in confluent mouse osteoblasts

The Neuromuscular Manifestations of Primary Hyperparathyroidism in Humans

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