High-Affinity Binding Sites for [3H]Verapamil in Cardiac Membranes

Ul, Hulthén; Landmann, Régine; Bürgisser, Ernst; Fr, Bühler

doi:10.1097/00005344-198200433-00006

Cited by 10 publications

(4 citation statements)

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“…Autoradiography reveals (Fig. 6) that pretreatment of neural crest cells (day 6 ) with verapamil(O.l5mM), which has highaffinity VDCC binding (Hulthen et al, 1982;Ehlert et al, 1982a,b), effectively blocks the subsequent binding of 3H-nitrendipine thereby corroborating the putative specificity of verapamil for the VDCC (Triggle and Ja nis, 1987).…”

Section: Autoradiographic Localization Of the -L-c$+ Channel With 3h-mentioning

confidence: 79%

“…a, b, x 300; c, x 250. ently essential for neural crest morphogenesis. Highaffinity binding of VDCCs with the phenylalkylamine verapamil blocks Ca2+ flux (Hulthen et al, 1982;Triggle and Janis, 1987;Panza et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…Verapamil was chosen as a VDCC probe because it exhibits selective high affinity binding (Ehlert et al, 1982a,b;Hulthen et al, 1982) and water solubility. Cultures were grown in the continuous presence of non-radioactive verapamil hydrochloride (Sigma, St. Louis, MO) in concentrations of 0.05, 0.10, 0.15 and 0.20mM and were assessed against controls for their ability to migrate and differentiate morphologically.…”

Section: Treatment With Verapamilmentioning

confidence: 99%

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Voltage‐dependent ‐L‐type Ca²⁺ channels participate in regulating neural crest migration and differentiation

Moran

1991

Am. J. Anat.

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General models of cell activation implicate Ca2+ conductance as pivotal in conveying transmembrane signals. During embryonic development, both cell migration and differentiation are influenced by changes in Ca2+; and, as a consequence, the modulation of Ca2+ is important in the control of many morphogenetic processes. Because Ca2+ conductance may be regulated at voltage-dependent Ca2+ channels (VD-CCs), we investigated whether neural crest cells develop VDCCs and, if so, whether they function in regulating migration and establishing cytomorphology. Autoradiography indicates that neural crest cells in vitro develop -L-type Ca2+ channels during migration and differentiation. Blockage of these channels by verapamil, both in vivo and in vitro, leads to a dramatic and reversible inhibition of neural crest migration. Alterations are manifest in vitro in cell-to-cell and cell-to-substratum contact and in the organization of the actin cytoskeleton. In whole embryos, verapamil or nifedipine inhibits pigment pattern formation. Moreover, blockage of the -L-type Ca2+ channels in whole embryos or cultures, after cells have already migrated and differentiated, results in a significant change in individual cell shape and in the overall pigment cell pattern, suggesting further that maintenance of the differentiated state also requires regulation at the -L-type Ca2+ channel. Since certain aspects of neural crest adhesion and cytoskeletal function are dependent on Ca2+, it is suggested that interactions that regulate the availability of Ca2+ through the VDCC may provide coordinate control of motile and adhesive interactions at the cell-substratum interface.

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Section: Autoradiographic Localization Of the -L-c$+ Channel With 3h-mentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Treatment With Verapamilmentioning

confidence: 99%

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Voltage‐dependent ‐L‐type Ca²⁺ channels participate in regulating neural crest migration and differentiation

Moran

1991

Am. J. Anat.

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“…Using classical saturation and displacement binding techniques at least two and probably three chemically-distinct types of saturable, stereospecific binding sites have now been identified. Some of these binding sites are highly selective for the dihydropyridine-based Ca2+ antagonists whilst others preferentially bind the diphenylalkylamines, including verapamil and gallopamil (Hulthen et al, 1982;Reynolds et al, 1983). Within each group, however, both low and high affinity binding sites have been identified and characterized.…”

Section: Receptors For the Ca2+ Antagonistsmentioning

confidence: 99%

Calcium antagonists and their mode of action: an historical overview.

Nayler¹,

Dillon²

1986

Brit J Clinical Pharma

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The Ca2+ antagonists are a novel group of drugs useful in management of a variety of cardiac disorders. They differ from one another in terms of their chemistry, tissue specificity and selectivity. As a group, however, they share the common property of slowing Ca2+ entry through voltage‐activated, ion‐selective channels. Some of them exhibit other properties, including that of interfering with Na+ transport. At least one of them, diltiazem, has an intracellular action. Specific high and low affinity binding sites have been identified for two of the major groups of Ca2+‐antagonists, with the binding sites for verapamil and its derivatives being distinct from those which can be occupied by the dihydropyridines. The number (Bmax) and affinity (KD) of these binding sites changes under certain pathological conditions‐including a reduction in ischaemia and in spontaneous hypertension, an increase in the latter, at present, only demonstrated for the dihydropyridine binding sites. The sensitivity of a particular tissue to these drugs will depend upon a number of factors including the number of binding sites that are present, the contribution made by the Ca2+ entering through the voltage‐activated channels to the functioning of the tissue, and properties which are peculiar to a particular type of Ca2+ antagonist, for example, whether, as in the case of verapamil, they exhibit use‐dependence.

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Abnormalities of Vascular Ion Channels During Hypertension

Srivastava

MacMillan-Crow

Rhee

et al. 2016

Vascular Ion Channels in Physiology and Disease

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High-Affinity Binding Sites for [3H]Verapamil in Cardiac Membranes

Cited by 10 publications

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Voltage‐dependent ‐L‐type Ca²⁺ channels participate in regulating neural crest migration and differentiation

Voltage‐dependent ‐L‐type Ca²⁺ channels participate in regulating neural crest migration and differentiation

Calcium antagonists and their mode of action: an historical overview.

Abnormalities of Vascular Ion Channels During Hypertension

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High-Affinity Binding Sites for [3H]Verapamil in Cardiac Membranes

Cited by 10 publications

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Voltage‐dependent ‐L‐type Ca2+ channels participate in regulating neural crest migration and differentiation

Voltage‐dependent ‐L‐type Ca2+ channels participate in regulating neural crest migration and differentiation

Calcium antagonists and their mode of action: an historical overview.

Abnormalities of Vascular Ion Channels During Hypertension

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Product

Resources

About

Voltage‐dependent ‐L‐type Ca²⁺ channels participate in regulating neural crest migration and differentiation

Voltage‐dependent ‐L‐type Ca²⁺ channels participate in regulating neural crest migration and differentiation