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Pathogenesis of Sleep-Disordered Breathing in Adults
Published in Susmita Chowdhuri, M Safwan Badr, James A Rowley, Control of Breathing during Sleep, 2022
Thomas M Tolbert, Indu Ayappa, David M Rapoport
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
Published in Irving H. Zucker, Joseph P. Gilmore, 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.
Fetal Circulation
Published in Miriam Katz, Israel Meizner, Vaclav Insler, Fetal Well-Being, 2019
Miriam Katz, Israel Meizner, Vaclav Insler
The effect of variations in blood chemistry on ventilation and blood circulation is mediated by the chemoreceptors. Chemoreceptor cells are located in the medulla oblongata, the aortic arch, and in the carotic sinus. The central chemoreceptors respond to changes in oxygen and carbon dioxide tension in the arterial blood or in the cerebrospinal fluid. In the adult a drop in oxygen concentration and/or rise in CO2 will trigger tachycardia and a increase in arterial blood pressure — both of them being protective mechanisms, attempting to increase blood circulation in order to improve oxygen supply.
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).
Sleep apnea and atrial fibrillation: challenges in clinical and translational research
Published in Expert Review of Cardiovascular Therapy, 2022
Benedikt Linz, Julie Norup Hertel, Jeroen Hendriks, Arnela Saljic, Dobromir Dobrev, Mathias Baumert, Thomas Jespersen, Dominik Linz
Even though most AF patients suffer predominantly from obstructive sleep apnea (OSA) and single obstructive respiratory events are described to increase AF-susceptibility, central sleep apnea has also been associated with AF. The most common cause for central sleep apnea is congestive heart failure [31]. In heart failure patients, increased sensitivity of chemoreceptors, pulmonary congestion, and slowing in circulation may impair regulated respiratory control and predispose for central apneic events [32–34]. Additionally, a change in posture at night from upright to supine is associated with a prominent distribution of body fluid from the lower body part to the chest and neck area, also called rostral shift [35]. This is associated with an increase in neck volume, which increases the risk for upper airway collapsibility. Moreover, heart failure is associated with increased atrial volume and stretch and reduced repolarizing potassium currents, which might contribute to early or late afterdepolarizations, thus increasing AF-trigger formation [36].
Dopamine β hydroxylase as a potential drug target to combat hypertension
Published in Expert Opinion on Investigational Drugs, 2020
Sanjay Kumar Dey, Manisha Saini, Pankaj Prabhakar, Suman Kundu
The arterial baro- and chemo-reflexes are negative feedback mechanisms to maintain the beat-to-beat homeostasis in ABP [21]. Sudden change in ABP is detected by baroreceptors in the circulatory walls of the carotid sinus and aortic arch. These afferent baroreceptors then induce a sympatho-inhibitory reflex, known as baroreflex from carotid sinus and aorta using glossopharyngeal and vagus nerves, respectively, toward NTS and normalizes BP by adjusting cardiac output and vascular resistance [22–24]. In case of chronic hypertension, baroreceptors loses sensitivity and remains unable to prevent sudden variation in BP [22–24]. On the other hand, chemoreflexes are induced by the chemoreceptors which sense the changes in arterial PO2, PCO2, and pH at their distinct vassal locations in the carotid bodies and aortic bodies [18,23]. Respiratory center in the brain is stimulated by chemoreflex due to decrease in PO2 and pH or increase in PCO2, which in turn induces the sympathetic outflow. In obstructive sleep apnea patients, repeated stimulation of chemoreflex by chronic hypoxia and hypercapnia increases the chance of hypertension [21,25].