scholarly journals A role for nitric oxide in hypoxia-induced activation of cardiac KATP channels in goldfish (Carassius auratus)

2003 ◽  
Vol 206 (22) ◽  
pp. 4057-4065 ◽  
Author(s):  
J. S. Cameron
Keyword(s):  
Nitric Oxide ◽  
Carassius Auratus ◽  
Katp Channels ◽  
Goldfish Carassius Auratus

scholarly journals Mitochondrial KATP channels stabilize intracellular Ca2+ during hypoxia in retinal horizontal cells of goldfish (Carassius auratus)

2021 ◽  
Author(s):  
Michael W. Country ◽  
Michael G. Jonz
Keyword(s):  
Carassius Auratus ◽  
Katp Channels ◽  
Horizontal Cells ◽  
Hypoxia Tolerance ◽  
Dependent Manner ◽  
Cellular Mechanisms ◽  
Atp Production ◽  
Goldfish Carassius Auratus ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Mitochondrial Katp Channels

Neurons of the retina require oxygen to survive. In hypoxia, neuronal ATP production is impaired, ATP-dependent ion pumping is reduced, transmembrane ion gradients are dysregulated, and [Ca2+]i increases enough to trigger excitotoxic cell death. Central neurons of the common goldfish (Carassius auratus) are hypoxia-tolerant, but little is known about how goldfish retinas withstand hypoxia. To study the cellular mechanisms of hypoxia tolerance, we isolated retinal interneurons (horizontal cells; HCs), and measured intracellular Ca2+ concentration ([Ca2+]i) with Fura-2. Goldfish HCs maintained [Ca2+]i throughout 1 h of hypoxia, whereas [Ca2+]i increased irreversibly in HCs of the hypoxia-sensitive rainbow trout (Oncorhynchus mykiss) with just 20 min of hypoxia. Our results suggest mitochondrial ATP-dependent K+ channels (mKATP) are necessary to stabilize [Ca2+]i throughout hypoxia. In goldfish HCs, [Ca2+]i increased when mKATP was blocked with glibenclamide or 5-HD, whereas an mKATP agonist (diazoxide) prevented [Ca2+]i from increasing in hypoxia in trout HCs. We showed that hypoxia protects goldfish HCs via mKATP channels. Glycolytic inhibition with 2-deoxyglucose increased [Ca2+]i, which was rescued by hypoxia in an mKATP-dependent manner. We found no evidence of plasmalemmal KATP channels in patch-clamp experiments. Instead, we confirmed the involvement of KATP in mitochondria with TMRE imaging, as hypoxia rapidly (<5 min) depolarized mitochondria in an mKATP-sensitive manner. We conclude that mKATP channels initiate a neuroprotective pathway in goldfish HCs to maintain [Ca2+]i and avoid excitotoxicity in hypoxia. This model provides novel insight into the cellular mechanisms of hypoxia tolerance in the retina.

scholarly journals The Hypoxia Tolerance of the Goldfish (Carassius auratus) Heart: The NOS/NO System and Beyond

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 555 ◽  
Author(s):  
Mariacristina Filice ◽  
Rosa Mazza ◽  
Serena Leo ◽  
Alfonsina Gattuso ◽  
Maria Carmela Cerra ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carassius Auratus ◽  
Ex Vivo ◽  
Acute Hypoxia ◽  
Protein S ◽  
Elisa Test ◽  
Hypoxia Tolerance ◽  
No Production ◽  
Goldfish Carassius Auratus ◽  
Enhanced Expression

The extraordinary capacity of the goldfish (Carassius auratus) to increase its cardiac performance under acute hypoxia is crucial in ensuring adequate oxygen supply to tissues and organs. However, the underlying physiological mechanisms are not yet completely elucidated. By employing an ex vivo working heart preparation, we observed that the time-dependent enhancement of contractility, distinctive of the hypoxic goldfish heart, is abolished by the Nitric Oxide Synthase (NOS) antagonist L-NMMA, the Nitric Oxide (NO) scavenger PTIO, as well as by the PI3-kinase (PI3-K) and sarco/endoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) pumps’ inhibition by Wortmannin and Thapsigargin, respectively. In goldfish hearts exposed to hypoxia, an ELISA test revealed no changes in cGMP levels, while Western Blotting analysis showed an enhanced expression of the phosphorylated protein kinase B (pAkt) and of the NADPH oxidase catalytic subunit Nox2 (gp91phox). A significant decrease of protein S-nitrosylation was observed by Biotin Switch assay in hypoxic hearts. Results suggest a role for a PI3-K/Akt-mediated activation of the NOS-dependent NO production, and SERCA2a pumps in the mechanisms conferring benefits to the goldfish heart under hypoxia. They also propose protein denitrosylation, and the possibility of nitration, as parallel intracellular events.

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