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Gaseous transmitter regulation of hypoxia-evoked catecholamine secretion from murine adrenal chromaffin cells.
J Neurophysiol. 2021 05 01; 125(5):1533-1542.JN

Abstract

Emerging evidence suggests that gaseous molecules, carbon monoxide (CO), and hydrogen sulfide (H2S) generated by heme oxygenase (HO)-2 and cystathionine γ-lyase (CSE), respectively, function as transmitters in the nervous system. Present study examined the roles of CO and H2S in hypoxia-induced catecholamine (CA) release from adrenal medullary chromaffin cells (AMCs). Studies were performed on AMCs from adult (≥6 wk of age) wild-type (WT), HO-2 null, CSE null, and HO-2/CSE double null mice of either gender. CA secretion was determined by carbon fiber amperometry and [Ca2+]i by microflurometry using Fura-2. HO-2- and CSE immunoreactivities were seen in WT AMC, which were absent in HO-2 and CSE null mice. Hypoxia (medium Po2 30-38 mmHg) evoked CA release and elevated [Ca2+]i. The magnitude of hypoxic response was greater in HO-2 null mice and in HO inhibitor-treated WT AMC compared with controls. H2S levels were elevated in HO-2 null AMC. Either pharmacological inhibition or genetic deletion of CSE prevented the augmented hypoxic responses of HO-2 null AMC and H2S donor rescued AMC responses to hypoxia in HO-2/CSE double null mice. CORM3, a CO donor, prevented the augmented hypoxic responses in WT and HO-2 null AMC. CO donor reduced H2S levels in WT AMC. The effects of CO donor were blocked by either ODQ or 8pCT, inhibitors of soluble guanylyl cyclase (SGC) or protein kinase G, respectively. These results suggest that HO-2-derived CO inhibits hypoxia-evoked CA secretion from adult murine AMC involving soluble guanylyl cyclase (SGC)-protein kinase G (PKG)-dependent regulation of CSE-derived H2S.NEW & NOTEWORTHY Catecholamine secretion from adrenal chromaffin cells is an important physiological mechanism for maintaining homeostasis during hypoxia. Here, we delineate carbon monoxide (CO)-sensitive hydrogen sulfide (H2S) signaling as an important mediator of hypoxia-induced catecholamine secretion from murine adrenal chromaffin cells. Heme oxygenase-2 derived CO is a physiological inhibitor of catcholamince secretion by hypoxia and the effects of CO involve inhibition of cystathionine γ-lyase-derived H2S production through soluble guanylyl cyclase-protein kinase G signaling cascade.

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Authors+Show Affiliations

Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois.

Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois.

Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois.

Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois.

Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois.

Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois.

Department of Neuroscience, Physiology and Pharmacology, Biological Science Division, University of Chicago, Chicago, Illinois.

Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, University of Chicago, Chicago, Illinois.

MeSH

AnimalsCarbon MonoxideCatecholaminesChromaffin CellsCystathionine gamma-LyaseFemaleHeme Oxygenase (Decyclizing)Hydrogen SulfideHypoxiaMaleMiceMice, Inbred C57BLMice, TransgenicSignal Transduction

Pub Type(s)

Journal Article

Research Support, N.I.H., Extramural

Language

eng

PubMed ID

33729866

Citation

Gridina, Anna, et al. "Gaseous Transmitter Regulation of Hypoxia-evoked Catecholamine Secretion From Murine Adrenal Chromaffin Cells." Journal of Neurophysiology, vol. 125, no. 5, 2021, pp. 1533-1542.

Gridina A, Su X, Khan SA, et al. Gaseous transmitter regulation of hypoxia-evoked catecholamine secretion from murine adrenal chromaffin cells. J Neurophysiol. 2021;125(5):1533-1542.

Gridina, A., Su, X., Khan, S. A., Peng, Y. J., Wang, B., Nanduri, J., Fox, A. P., & Prabhakar, N. R. (2021). Gaseous transmitter regulation of hypoxia-evoked catecholamine secretion from murine adrenal chromaffin cells. Journal of Neurophysiology, 125(5), 1533-1542. https://doi.org/10.1152/jn.00669.2020

Gridina A, et al. Gaseous Transmitter Regulation of Hypoxia-evoked Catecholamine Secretion From Murine Adrenal Chromaffin Cells. J Neurophysiol. 2021 05 1;125(5):1533-1542. PubMed PMID: 33729866.

* Article titles in AMA citation format should be in sentence-case

TY - JOUR T1 - Gaseous transmitter regulation of hypoxia-evoked catecholamine secretion from murine adrenal chromaffin cells. AU - Gridina,Anna, AU - Su,Xiaoyu, AU - Khan,Shakil A, AU - Peng,Ying-Jie, AU - Wang,Benjamin, AU - Nanduri,Jayasri, AU - Fox,Aaron P, AU - Prabhakar,Nanduri R, Y1 - 2021/03/17/ PY - 2021/3/18/pubmed PY - 2022/1/11/medline PY - 2021/3/17/entrez KW - adrenal medullary chromaffin cells KW - cystathionine β-synthase KW - hypoxia KW - protein kinase G KW - soluble guanylyl cyclase SP - 1533 EP - 1542 JF - Journal of neurophysiology JO - J Neurophysiol VL - 125 IS - 5 N2 - Emerging evidence suggests that gaseous molecules, carbon monoxide (CO), and hydrogen sulfide (H2S) generated by heme oxygenase (HO)-2 and cystathionine γ-lyase (CSE), respectively, function as transmitters in the nervous system. Present study examined the roles of CO and H2S in hypoxia-induced catecholamine (CA) release from adrenal medullary chromaffin cells (AMCs). Studies were performed on AMCs from adult (≥6 wk of age) wild-type (WT), HO-2 null, CSE null, and HO-2/CSE double null mice of either gender. CA secretion was determined by carbon fiber amperometry and [Ca2+]i by microflurometry using Fura-2. HO-2- and CSE immunoreactivities were seen in WT AMC, which were absent in HO-2 and CSE null mice. Hypoxia (medium Po2 30-38 mmHg) evoked CA release and elevated [Ca2+]i. The magnitude of hypoxic response was greater in HO-2 null mice and in HO inhibitor-treated WT AMC compared with controls. H2S levels were elevated in HO-2 null AMC. Either pharmacological inhibition or genetic deletion of CSE prevented the augmented hypoxic responses of HO-2 null AMC and H2S donor rescued AMC responses to hypoxia in HO-2/CSE double null mice. CORM3, a CO donor, prevented the augmented hypoxic responses in WT and HO-2 null AMC. CO donor reduced H2S levels in WT AMC. The effects of CO donor were blocked by either ODQ or 8pCT, inhibitors of soluble guanylyl cyclase (SGC) or protein kinase G, respectively. These results suggest that HO-2-derived CO inhibits hypoxia-evoked CA secretion from adult murine AMC involving soluble guanylyl cyclase (SGC)-protein kinase G (PKG)-dependent regulation of CSE-derived H2S.NEW & NOTEWORTHY Catecholamine secretion from adrenal chromaffin cells is an important physiological mechanism for maintaining homeostasis during hypoxia. Here, we delineate carbon monoxide (CO)-sensitive hydrogen sulfide (H2S) signaling as an important mediator of hypoxia-induced catecholamine secretion from murine adrenal chromaffin cells. Heme oxygenase-2 derived CO is a physiological inhibitor of catcholamince secretion by hypoxia and the effects of CO involve inhibition of cystathionine γ-lyase-derived H2S production through soluble guanylyl cyclase-protein kinase G signaling cascade. SN - 1522-1598 UR - https://www.unboundmedicine.com/medline/citation/33729866/Gaseous_transmitter_regulation_of_hypoxia_evoked_catecholamine_secretion_from_murine_adrenal_chromaffin_cells_ DB - PRIME DP - Unbound Medicine ER -