ArticleACS chemical neuroscience2013
Increased catecholamine secretion from single adrenal chromaffin cells in DOCA-salt hypertension is associated with potassium channel dysfunction.
Article in ACS chemical neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A KBiomolecules · 2026Article
- Wnt/β-catenin signaling in the adrenal glands of rats in various types of experimental hypertension.Endocrine connections · 2022Article
- TNFα increases tyrosine hydroxylase expression in human monocytes.NPJ Parkinson's disease · 2021Article
- Central Noradrenergic Agonists in the Treatment of Ischemic Stroke-an Overview.Translational stroke research · 2020Review
- Where Is Dopamine and how do Immune Cells See it?: Dopamine-Mediated Immune Cell Function in Health and Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- Inflammatory Signaling in Hypertension: Regulation of Adrenal Catecholamine Biosynthesis.Frontiers in endocrinology · 2018Review
- MicroRNA exocytosis by large dense-core vesicle fusion.Scientific reports · 2017Article
- Enhanced Ca(2+)-induced Ca(2+) release from intracellular stores contributes to catecholamine hypersecretion in adrenal chromaffin cells from spontaneously hypertensive rats.Pflugers Archiv : European journal of physiology · 2015Article
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Abstract
The mechanism of catecholamine release from single adrenal chromaffin cells isolated from normotensive and DOCA-salt hypertensive rats was investigated. These cells were used as a model for sympathetic nerves to better understand how exocytotic release of catecholamines is altered in this model of hypertension. Catecholamine secretion was evoked by local application of acetylcholine (1 mM) or high K+ (70 mM), and continuous amperometry was used to monitor catecholamine secretion as an oxidative current. The total number of catecholamine molecules secreted from a vesicle, the total number of vesicles fusing and secreting, and the duration of secretion in response to a stimulus were all significantly greater for chromaffin cells from hypertensive rats as compared to normotensive controls. The greater catecholamine secretion from DOCA-salt cells results, at least in part, from functionally impaired large conductance, Ca2+-activated (BK) and ATP-sensitive K+ channels. This work reveals that there is altered vesicular release of catecholamines from these cells (and possibly from perivascular sympathetic nerves) and this may contribute to increased vasomotor tone in DOCA-salt hypertension.
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