Role of intracellular calcium in peroxide-induced potentiation of norepinephrine release from bovine isolated irides

Catherine A. Opere; Sunny E. Ohia

doi:10.1016/S0306-3623(98)00090-1

Role of intracellular calcium in peroxide-induced potentiation of norepinephrine release from bovine isolated irides

Catherine A. Opere, Sunny E. Ohia

Department of Pharmacy Sciences

Research output: Contribution to journal › Article

7 Scopus citations

Abstract

1. BAPTA AM (10 μM), thapsigargin (10 μM), ruthenium red (30 μM) and oligomycin (30 μM) inhibited field-stimulated [³H]NE release from bovine isolated irides by 54%, 30%, 30% and 26%, respectively. 2. Both BAPTA AM and thapsigargin had no significant effect (P>0.05) on H₂O₂-induced potentiation of evoked [³H]NE release. 3. Ruthenium red prevented (but oligomycin enhanced) H₂O₂-induced enhancement of evoked [³H]NE release. 4. We conclude that, although intracellular calcium participates in field-stimulation evoked [³H]NE release from bovine isolated irides, only the mitochondrial pool of calcium may be involved in peroxide-induced enhancement of sympathetic neurotransmission. Copyright (C) 1998 Elsevier Science Inc.

Original language	English (US)
Pages (from-to)	793-798
Number of pages	6
Journal	General Pharmacology
Volume	31
Issue number	5
DOIs	https://doi.org/10.1016/S0306-3623(98)00090-1
State	Published - Nov 1 1998

All Science Journal Classification (ASJC) codes

Pharmacology

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Opere, C. A., & Ohia, S. E. (1998). Role of intracellular calcium in peroxide-induced potentiation of norepinephrine release from bovine isolated irides. General Pharmacology, 31(5), 793-798. https://doi.org/10.1016/S0306-3623(98)00090-1

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abstract = "1. BAPTA AM (10 μM), thapsigargin (10 μM), ruthenium red (30 μM) and oligomycin (30 μM) inhibited field-stimulated [3H]NE release from bovine isolated irides by 54%, 30%, 30% and 26%, respectively. 2. Both BAPTA AM and thapsigargin had no significant effect (P>0.05) on H2O2-induced potentiation of evoked [3H]NE release. 3. Ruthenium red prevented (but oligomycin enhanced) H2O2-induced enhancement of evoked [3H]NE release. 4. We conclude that, although intracellular calcium participates in field-stimulation evoked [3H]NE release from bovine isolated irides, only the mitochondrial pool of calcium may be involved in peroxide-induced enhancement of sympathetic neurotransmission. Copyright (C) 1998 Elsevier Science Inc.",

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N2 - 1. BAPTA AM (10 μM), thapsigargin (10 μM), ruthenium red (30 μM) and oligomycin (30 μM) inhibited field-stimulated [3H]NE release from bovine isolated irides by 54%, 30%, 30% and 26%, respectively. 2. Both BAPTA AM and thapsigargin had no significant effect (P>0.05) on H2O2-induced potentiation of evoked [3H]NE release. 3. Ruthenium red prevented (but oligomycin enhanced) H2O2-induced enhancement of evoked [3H]NE release. 4. We conclude that, although intracellular calcium participates in field-stimulation evoked [3H]NE release from bovine isolated irides, only the mitochondrial pool of calcium may be involved in peroxide-induced enhancement of sympathetic neurotransmission. Copyright (C) 1998 Elsevier Science Inc.

AB - 1. BAPTA AM (10 μM), thapsigargin (10 μM), ruthenium red (30 μM) and oligomycin (30 μM) inhibited field-stimulated [3H]NE release from bovine isolated irides by 54%, 30%, 30% and 26%, respectively. 2. Both BAPTA AM and thapsigargin had no significant effect (P>0.05) on H2O2-induced potentiation of evoked [3H]NE release. 3. Ruthenium red prevented (but oligomycin enhanced) H2O2-induced enhancement of evoked [3H]NE release. 4. We conclude that, although intracellular calcium participates in field-stimulation evoked [3H]NE release from bovine isolated irides, only the mitochondrial pool of calcium may be involved in peroxide-induced enhancement of sympathetic neurotransmission. Copyright (C) 1998 Elsevier Science Inc.

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