ArticleThe Journal of physiology2007
Increased secretory capacity of mouse adrenal chromaffin cells by chronic intermittent hypoxia: involvement of protein kinase C.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Molecular crosstalk between gas transmitters and catecholamine biosynthesis pathways: a narrative review.Medical gas research · 2027Review
- Histone Deacetylase 5 Is an Early Epigenetic Regulator of Intermittent Hypoxia Induced Sympathetic Nerve Activation and Blood Pressure.Frontiers in physiology · 2021Article
- Article
- Neural Activation of Molecular Circuitry in Intermittent Hypoxia.Current opinion in physiology · 2019Article
- Inflammatory Signaling in Hypertension: Regulation of Adrenal Catecholamine Biosynthesis.Frontiers in endocrinology · 2018Review
- Carotid body chemoreflex: a driver of autonomic abnormalities in sleep apnoea.Experimental physiology · 2016Review
- Neuromolecular mechanisms mediating the effects of chronic intermittent hypoxia on adrenal medulla.Respiratory physiology & neurobiology · 2015Review
- Carotid Body Chemoreflex Mediates Intermittent Hypoxia-Induced Oxidative Stress in the Adrenal Medulla.Advances in experimental medicine and biology · 2015Article
- HIF-1α activation by intermittent hypoxia requires NADPH oxidase stimulation by xanthine oxidase.PloS one · 2015Article
- Recent insights on circulating catecholamines in hypertension.Current hypertension reports · 2014Review
- Melatonin attenuates intermittent hypoxia-induced lipid peroxidation and local inflammation in rat adrenal medulla.International journal of molecular sciences · 2014Article
- Regulation of hypoxia-inducible factor-α isoforms and redox state by carotid body neural activity in rats.The Journal of physiology · 2014Article
- Neuropeptide y gates a stress-induced, long-lasting plasticity in the sympathetic nervous system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Mutual antagonism between hypoxia-inducible factors 1α and 2α regulates oxygen sensing and cardio-respiratory homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Sympatho-adrenal activation by chronic intermittent hypoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Review
- Cocaine facilitates PKC maturation by upregulating its phosphorylation at the activation loop in rat striatal neurons in vivo.Brain research · 2012Article
- Hypoxia-inducible factor 1 mediates increased expression of NADPH oxidase-2 in response to intermittent hypoxia.Journal of cellular physiology · 2011Article
- NADPH oxidase 2 mediates intermittent hypoxia-induced mitochondrial complex I inhibition: relevance to blood pressure changes in rats.Antioxidants & redox signaling · 2011Article
- Intermittent hypoxia augments acute hypoxic sensing via HIF-mediated ROS.Respiratory physiology & neurobiology · 2010Review
- Mechanisms of sympathetic activation and blood pressure elevation by intermittent hypoxia.Respiratory physiology & neurobiology · 2010Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have shown that catecholamine secretion from the adrenal medulla plays a critical role in chronic intermittent hypoxia (CIH)-induced alterations in cardiovascular function. In the present study we examined the cellular mechanisms associated with the effects of CIH on adrenal chromaffin cell catecholamine secretion. Experiments were performed on adult male mice (C57/BL6) that were exposed to 1-4 days of CIH or to normoxia. Perforated patch electrical capacitance recordings were performed on freshly prepared adrenal medullary slices that permit separating the chromaffin cell secretion from sympathetic input. CIH resulted in a significant increase in the readily releasable pool (RRP) of secretory granules, and decreased stimulus-evoked Ca(2+) influx. Continuous hypoxia (CH) either for 2.5 h (equivalent to hypoxic duration accumulated over 4 days of CIH) or for 4 days were ineffective in evoking changes in the RRP and Ca(2+) influx. CIH activated PKC in adrenal medullae as evidenced by increased phosphorylation of PKC at Thr(514) and PKC inhibitors prevented CIH-induced increases in the RRP and restored stimulus-evoked attenuation of Ca(2+) influx. CIH resulted in elevated thio-barbituric acid reactive substances (TBARSs, an index of oxidized proteins) and an antioxidant prevented CIH-induced changes in the RRP, suggesting the involvement of reactive oxygen species (ROS). These results demonstrate that CIH increases the RRP in adrenal chromaffin cells via ROS-mediated activation of PKC and suggest that CIH can directly affect the secretory capacity of chromaffin cells and contribute, in part, to elevated catecholamine levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.