Pathogenesis of Sleep-Disordered Breathing in Adults
Susmita Chowdhuri, M Safwan Badr, James A Rowley in Control of Breathing during Sleep, 2022
Specialized structures called chemoreceptors monitor local O2 and CO2 partial pressures (PaO2 and PaCO2) and provide signals to the brainstem, which integrates these afferent inputs to determine output to the muscles of ventilation, including the respiratory pump (principally the diaphragm) and the muscles of the upper airway. Central chemoreceptors are located in the central nervous system, principally in the medulla, and are sensitive to changes in CO2 and pH. Peripheral chemoreceptors are components of the peripheral nervous system, located principally at the bifurcations of the carotid arteries (i.e. the carotid bodies) and in the aorta. They mainly respond to local hypoxia, but may also increase their activity in conditions of low pH, elevated PaCO2, or low blood flow (11).
Atrial Receptors
Irving H. Zucker, Joseph P. Gilmore in Reflex Control of the Circulation, 2020
The activity of unmyelinated vagal afferents frequently does not possess a cardiac rhythm (Coleridge et al., 1973; Kappagoda et al., 1979). Atrial afferents, like ventricular afferents, can be strongly excited by injection into the coronary arteries of various chemicals including veratridine, phenyl diguanide, capsaicin, bradykinin, and prostaglandins. Baker et al. (1979) suggested that nonmyelinated cardiac afferents might be classified into those that are predominantly chemosensitive and those that are mechanosensitive. However, it should be emphasized that such a classification is only approximate since most receptors respond to both mechanical and chemical stimuli. Furthermore, it should be noted that these receptors are not really chemoreceptors since they do not respond directly to physiological changes in blood gases.
Nonobstructive Sleep Patterns in Children
Mark A. Richardson, Norman R. Friedman in Clinician’s Guide to Pediatric Sleep Disorders, 2016
Taken to a sufficient altitude, everyone will show periodic breathing when they sleep. Most people who ascend from sea level to 4000 m (13,000 ft) will exhibit this pattern, but certain individuals appear predisposed to developing periodic breathing at lower altitudes because of the increased chemoresponsiveness to hypoxia. The hypoxic ventilatory response of these people induces hyperventilation in response to the decreased oxygen tension at high altitude. The body’s response to the hyperventilation-induced drop in CO2 tension is a period of apnea during which the CO2 level rises. When the CO2 level exceeds the apnea threshold, the hypoxic ventilatory response again induces hyperventilation and the cycle starts anew. Affected individuals have a disrupted sleep pattern with frequent arousals and restlessness. Periodic breathing in infants brought to altitude may become more pronounced and have greater swings in oxygen saturations (9). There are no specific treatments. Infants born at high-altitude may require a short period on home oxygen therapy to avoid significant desaturations. Older children and adults rarely need oxygen, but a slow ascent will minimize the sleep disruption. The abnormal sleep usually improves as the chemoreceptors reset and the person acclimates to altitude. There is no clear association between high-altitude periodic breathing and other diseases of high altitude such as acute mountain sickness, high-altitude pulmonary edema, or high-altitude cerebral edema (10,11).
Novel approaches: targeting sympathetic outflow in the carotid sinus
Published in Blood Pressure, 2023
Dagmara Hering, Krzysztof Narkiewicz
The peripheral arterial chemoreceptors are located in the carotid and aortic bodies, and respond primarily to changes in oxygen levels (hypoxia), while central chemoreceptors are located on the ventral surface of the medulla oblongata and primarily respond to changes in carbon dioxide (CO2) levels (hypercapnia) [10,12]. Activation of afferent impulses from the carotid chemoreceptors in response to hypoxia leads to simultaneous activation of the cardiorespiratory centre in the medulla oblongata (synapsing to neurons in the caudal, commissural nucleus tractus solitarius, NTS) resulting in simultaneous hyperventilation and selective peripheral vasoconstriction (increased sympathetic activity to blood vessels). At the same time, hyperventilation through a stretch of thoracic afferents elicits an inhibitory or buffering influence on the autonomic response to hypoxaemia resulting in bradycardia, mediated by increased cardiac vagal outflow (Figure 2).
Pediatric neuropsychiatric syndromes associated with infection and microbiome alterations: clinical findings, possible role of the mucosal epithelium, and strategies for the development of new animal models
Published in Expert Opinion on Drug Discovery, 2022
Kurt Leroy Hoffman, Hugo Cano-Ramírez
3) Both respiratory and gut epithelia receive vagal sensory afferents and motor efferents. As described in the previous sections, vagal sensory afferents of the gut epithelium detect a variety of mechanical and chemical stimuli. Similarly, vagal sensory afferents of the respiratory system comprise a variety of mechanoreceptors (stretch and touch) and chemoreceptors (nocioceptive) [106]. Stimulation of these afferents evokes an ‘urge to cough’ and activity in a number of brain regions [107]. Given that the vagal nerve carries afferent and efferent fibers that mediate airway and esophageal reflexes, it is notable that food restriction symptoms in PANS often involved fear of choking, fear of vomiting, refusal to swallow own saliva, as well as fears of contamination from germs, poisons, or allergens [23].
C. elegans: a sensible model for sensory biology
Published in Journal of Neurogenetics, 2020
Adam J. Iliff, X.Z. Shawn Xu
Beyond mechanical stimuli, C. elegans also tastes and smells via multiple chemoreceptor families. Worm chemosensation has been studied extensively and the neural circuits and receptors responsible have been described in exquisite detail (Bargmann, 2006). Bargmann and colleagues led the identification of the large chemoreceptor family of G-protein couple receptors (GPCRs) with the discovery of the GPCR ODR-10 and its odorant ligand diacetyl (Sengupta, Chou, & Bargmann, 1996; Troemel, Chou, Dwyer, Colbert, & Bargmann, 1995). Of course, mammalian olfactory receptors are also known to be GPCRs (Buck & Axel, 1991). In addition, the transduction pathway is G protein signaling coupled to either cyclic nucleotide-gated (CNG) channels (TAX-4/TAX-2) or TRP channels (OSM-9/OCR-2 proteins). Both of these transduction mechanisms are also found in mammalian olfactory neurons. In addition to odorants and tastants, we now know that worms can detect a wide range of chemicals, including the physiologically relevant gases oxygen and carbon dioxide via a separate set of sensory neurons with guanylate cyclases as molecular sensors (Bargmann, 2006; Bretscher, Busch, & de Bono, 2008; Hallem & Sternberg, 2008). Worm sensory neurons also confer sensitivity to the pH and osmolarity of solutions (Bargmann, 2006; Wang, Li, Liu, Liu, & Xu, 2016), allowing worms to avoid harmful environments.