Plasmalemmal dihydropyridine receptors modify the function of subplasmalemmal inositol 1,4,5-trisphosphate receptors: a hypothesis

A. Spät, T. Rohács, L. Hunyady

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11 Citations (Scopus)

Abstract

Experimental observations on rat glomerulosa cells inspired a model which postulates that plasmalemmal dihydropyridine receptors are in juxtaposition and interaction with inositol 1,4,5-trisphosphate receptors in subplasmalemmal calciosomes. Activation of dihydropyridine receptors promotes the Ca2+ releasing effect of inositol 1,4,5-trisphosphate. The most important observations compatible with the model are the following: (1) angiotensin II does not influence Ca2+ influx during the peak phase of Ca2+ signal; (2) dihydropyridine drugs modify the initial peak of the Ca2+ signal induced by angiotensin II; (3) inhibitors of the dihydropyridine receptor reduce the initial Ca2+ signal also in the presence of 5 mM Ni2+, an inhibitor of voltage dependent Ca2+ influx; and (4) changes in extracellular K+ concentration within the physiological range also modify the cytoplasmic Ca2+ response to angiotensin II.

Original languageEnglish
Pages (from-to)431-437
Number of pages7
JournalCell Calcium
Volume15
Issue number5
DOIs
Publication statusPublished - 1994

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Inositol 1,4,5-Trisphosphate Receptors
L-Type Calcium Channels
Angiotensin II
Inositol 1,4,5-Trisphosphate
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Cell Biology
  • Endocrinology

Cite this

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title = "Plasmalemmal dihydropyridine receptors modify the function of subplasmalemmal inositol 1,4,5-trisphosphate receptors: a hypothesis",
abstract = "Experimental observations on rat glomerulosa cells inspired a model which postulates that plasmalemmal dihydropyridine receptors are in juxtaposition and interaction with inositol 1,4,5-trisphosphate receptors in subplasmalemmal calciosomes. Activation of dihydropyridine receptors promotes the Ca2+ releasing effect of inositol 1,4,5-trisphosphate. The most important observations compatible with the model are the following: (1) angiotensin II does not influence Ca2+ influx during the peak phase of Ca2+ signal; (2) dihydropyridine drugs modify the initial peak of the Ca2+ signal induced by angiotensin II; (3) inhibitors of the dihydropyridine receptor reduce the initial Ca2+ signal also in the presence of 5 mM Ni2+, an inhibitor of voltage dependent Ca2+ influx; and (4) changes in extracellular K+ concentration within the physiological range also modify the cytoplasmic Ca2+ response to angiotensin II.",
author = "A. Sp{\"a}t and T. Roh{\'a}cs and L. Hunyady",
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T1 - Plasmalemmal dihydropyridine receptors modify the function of subplasmalemmal inositol 1,4,5-trisphosphate receptors

T2 - a hypothesis

AU - Spät, A.

AU - Rohács, T.

AU - Hunyady, L.

PY - 1994

Y1 - 1994

N2 - Experimental observations on rat glomerulosa cells inspired a model which postulates that plasmalemmal dihydropyridine receptors are in juxtaposition and interaction with inositol 1,4,5-trisphosphate receptors in subplasmalemmal calciosomes. Activation of dihydropyridine receptors promotes the Ca2+ releasing effect of inositol 1,4,5-trisphosphate. The most important observations compatible with the model are the following: (1) angiotensin II does not influence Ca2+ influx during the peak phase of Ca2+ signal; (2) dihydropyridine drugs modify the initial peak of the Ca2+ signal induced by angiotensin II; (3) inhibitors of the dihydropyridine receptor reduce the initial Ca2+ signal also in the presence of 5 mM Ni2+, an inhibitor of voltage dependent Ca2+ influx; and (4) changes in extracellular K+ concentration within the physiological range also modify the cytoplasmic Ca2+ response to angiotensin II.

AB - Experimental observations on rat glomerulosa cells inspired a model which postulates that plasmalemmal dihydropyridine receptors are in juxtaposition and interaction with inositol 1,4,5-trisphosphate receptors in subplasmalemmal calciosomes. Activation of dihydropyridine receptors promotes the Ca2+ releasing effect of inositol 1,4,5-trisphosphate. The most important observations compatible with the model are the following: (1) angiotensin II does not influence Ca2+ influx during the peak phase of Ca2+ signal; (2) dihydropyridine drugs modify the initial peak of the Ca2+ signal induced by angiotensin II; (3) inhibitors of the dihydropyridine receptor reduce the initial Ca2+ signal also in the presence of 5 mM Ni2+, an inhibitor of voltage dependent Ca2+ influx; and (4) changes in extracellular K+ concentration within the physiological range also modify the cytoplasmic Ca2+ response to angiotensin II.

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