ArticleExperimental physiology2019
Carotid bodies contribute to sympathoexcitation induced by acute salt overload.
Article in Experimental physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Neural Control of Tissue Perfusion: Emerging Evidence and Beyond.Current hypertension reports · 2026Review
- Feasibility and safety of repeated 23% hypertonic saline boluses for electrical impedance tomography contrast enhancement in anaesthetised horses.Frontiers in veterinary science · 2026Article
- Hypoxia sensing in the body: An update on the peripheral and central mechanisms.Experimental physiology · 2024Review
- Article
- COBrain structure & function · 2022Article
- The carotid body: A novel key player in neuroimmune interactions.Frontiers in immunology · 2022Review
- Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone.Frontiers in physiology · 2021Review
- Medullary Noradrenergic Neurons Mediate Hemodynamic Responses to Osmotic and Volume Challenges.Frontiers in physiology · 2021Article
- Hyperthermia and dehydration: their independent and combined influences on physiological function during rest and exercise.European journal of applied physiology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
NEW
findingsWhat is the central question of this study? Does carotid body input contribute to the hyperosmotic responses? What is the main finding and its importance? The response to NaCl overload is sympathorespiratory excitation. Eliminating the carotid body input reduced sympathoexcitation but did not affect the increase in phrenic burst frequency, whereas eliminating the hypothalamus prevented the tachypnoea and sympathoexcitation. We conclude that the carotid body inputs are essential for the full expression of the sympathetic activity during acute NaCl overload, whereas the tachypnoea depends on hypothalamic mechanisms. ABSTRACT: Acute salt excess activates central osmoreceptors, which trigger an increase in sympathetic and respiratory activity. The carotid bodies also respond to hyperosmolality of the extracellular compartment, but their contribution to the sympathoexcitatory and ventilatory responses to NaCl overload remains unknown. To evaluate their contribution to acute NaCl overload, we recorded thoracic sympathetic (tSNA), phrenic (PNA) and carotid sinus nerve activities in decorticate in situ preparations of male Holtzman rats (60-100 g) while delivering intra-arterial infusions of hyperosmotic NaCl (0.17, 0.3, 0.7, 1.5 and 2.0 mol l
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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.