Role of the Endoplasmic Reticulum and Mitochondria on Quantal Catecholamine Release from Chromaffin Cells of Control and Hypertensive Rats
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Here, we present the first study on the effects of compounds that interfere with calcium (Ca(2+)) handling by the endoplasmic reticulum (ER) and mitochondria on amperometrically measured quantal catecholamine release from single adrenal chromaffin cells of control and spontaneously hypertensive rats (SHRs). Acetylcholine (ACh) or K(+) pulses triggered spike bursts of secretion by Ca(2+) entry through Ca(2+) channels. ER Ca(2+) release triggered by a mixture of caffeine, ryanodine, and thapsigargin (CRT) or carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) (a mitochondrial protonophore) also caused bursts of secretory spikes. The spike bursts generated by ACh, K(+), CRT, and FCCP were 3 to 4 times longer in SHRs compared with control cells; furthermore, the individual spikes were faster and had 3-fold greater quantal size. In additional experiments, a 90-s treatment was made with CRT or FCCP to block Ca(2+) handling by the ER and mitochondria. In these conditions, the integrated spike burst responses elicited by ACh and K(+) were potentiated 2- to 3-fold in control and SHR cells. This suggests that variations in Ca(2+) entry and its subsequent redistribution into the ER and mitochondria are not responsible for the greater secretion seen in SHRs compared with control cells; rather, such differences seem to be due to greater quantal content of spike bursts and to greater quantal size of individual amperometric events.
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Use of CCCP or FCCP decreases the Ca2+ buffering capacity of mitochondria and increases global exocytosis in bovine and rat chromaffin cells but not in the same cell type in mice.
“In accordance with this theory, use of CCCP or FCCP decreases the Ca2+ buffering capacity of mitochondria and increases global exocytosis in bovine [164,165] and rat chromaffin cells [166] but not in the same cell type in mice [167], suggesting species differences.”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [166]
By decreasing the Ca2+ buffering capacity of mitochondria, CCCP or FCCP increases global exocytosis in chromaffin cells.
“By decreasing the Ca2+ buffering capacity of mitochondria, CCCP or FCCP increases global exocytosis in chromaffin cells [164,165,166].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [166]
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Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases
Demine, S., Renard, P., & Arnould, T. (2019) · Cells · doi:10.3390/cells8080795 · Cited by 476 · see citing works
“In accordance with this theory, use of CCCP or FCCP decreases the Ca2+ buffering capacity of mitochondria and increases global exocytosis in bovine [164,165] and rat chromaffin cells [166] but not in the same cell type in mice [167], suggesting species differences.”
MethodCaricati-Neto, A., Padín, J.-F., Silva-Junior, E.-D., Fernández-Morales, J.-C., de Diego, A.-M. G., Jurkiewicz, A., & García, A. G. (2013) · Physiological Reports · doi:10.1002/phy2.182 · Cited by 12 · see citing works
Self-citation
- Authors
- Miranda-Ferreira, R., de Pascual, R., Caricati-Neto, A., Gandía, L., Jurkiewicz, A., & García, A. G.
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 329
- Issue
- 1
- Pages
- 231-240
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W2139930416
- Cited by
- 35
- References
- 43
- Citations by year
- 2022: 3 · 2021: 3 · 2020: 1 · 2019: 5 · 2018: 3 · 2017: 1 · 2015: 4 · 2014: 1 · 2013: 5
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- green
- americanae.aecid.es
- Licence
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Americanae (AECID Library) (submittedVersion, other-oa)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Topics
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- mitochondrial calcium handling, chromaffin cells, adrenal medulla, spontaneously hypertensive rats, hypertension, calcium channels, caffeine, ryanodine, thapsigargin, FCCP, acetylcholine, spike bursts, secretory granules
- MeSH terms
- Animals, Caffeine, Calcium, Calcium Channel Agonists, Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone, Catecholamines, Cell Separation, Endoplasmic Reticulum, Enzyme Inhibitors, Hypertension, Mitochondria, Potassium, Rats, Inbred SHR, Ryanodine, Uncoupling Agents, Calcium Channels, Rats, Sprague-Dawley, Thapsigargin, Chromaffin Cells, Calcium Signaling, Rats
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