Arterial Chemoreceptors and Sympathetic Nerve Activity

Abstract

C hronic elevation in sympathetic nerve activity (SNA) is associated with the development and maintenance of certain types of hypertension 1 and contributes to the progression of chronic heart failure (CHF). 2 The mechanisms involved in sympathetic dysfunction in these disorders appear to be complex and multifactorial. A unified hypothesis is likely to encompass alterations in multiple autonomic reflex pathways, central integratory sites, and chemical mediators that control sympathetic outflow. For example, tonic restraint of sympathetic outflow by arterial and cardiopulmonary baroreflexes is depressed in CHF 2 and depressed or reset in hypertension. 3 Moreover, maladaptive changes also occur in the central nervous system at integrative sites for autonomic control in both disease processes. 4,5 It is also clear that sympathoexcitatory cardiac, 6 somatic, 7 and central/peripheral chemoreceptor reflexes 8 are enhanced in CHF and hypertension.Arterial chemoreceptors serve an important regulatory role in the control of alveolar ventilation, but they also exert a powerful influence on cardiovascular function. 9 Activation of arterial chemoreceptors by hypoxemia increases sympathetic outflow to systemic vascular beds to compensate for the direct vasodilating effects of hypoxia on these vessels and to redistribute blood flow to essential organs. In this review, we highlight relevant information that implicates the arterial chemoreflex as a contributory mechanism for the sympathetic hyperactivity in CHF and hypertension and illustrate proposed mechanisms for this altered function. The Sympathetic Response to Arterial Chemoreceptor ActivationArterial chemoreceptors located in the aortic and carotid bodies (CBs) respond to hypoxemia and hypercapnia. Because central chemoreceptors also respond to hypercapnia, hypoxia is typically used as a specific stimulus to arterial chemoreceptors. In some mammals, such as rats and rabbits, reflex responses to hypoxemia arise solely from the CB, whereas in other species, the aortic chemoreceptor contribution can be significant. However, it is not possible to experimentally separate the relative contribution of the aortic and CBs to reflex responses in conscious animals or humans. For these reasons, discussions on the arterial chemoreflex generally relate functionality to that of the CB, which has been more extensively studied. Glomus cells in the CB depolarize in response to hypoxia and release multiple putative neurotransmitters (including acetylcholine, serotonin, ATP, and substance P) that activate impulses in afferent fibers traveling to the medulla via the carotid sinus nerve. 10 Arterial chemoreceptor stimulation in freely breathing humans and conscious animals increases sympathetic vasoconstrictor outflow to muscle, splanchnic, and renal beds to elevate arterial pressure, and, in humans, increases cardiac sympathetic activity to increase heart rate and contractility. 9 There is preferential activation of sympathetic fibers going to the adrenal gland to increase norepinephrine but...

Hydrogen sulphide-related thiol metabolism and nutrigenetics in relation to hypertension in an elderly population

“…The contribution of this haem-containing enzyme to H 2 S generation likely decreases under conditions of hyperhomocysteinaemia; gasotransmitter synthesis is relatively insensitive to Hcy, indicating that cystathionine c-lyase is largely responsible for enhancing H 2 S generation under conditions of hyperhomocysteinaemia. These findings, it has been suggested, point to an important new role for cystathionine c-lyase in the thiol metabolome and Hcy management (Singh et al 2009) and, as the present data indicate, in contributing to a significant clinical phenotype associated with substantial rates of morbidity and mortality (Kearney et al 2005;Reynolds et al 2007;Inoue et al 2007;Elliott 2005;Schultz et al 2007;Paoletti et al 2006;Parnetti et al 2004;Zylberstein et al 2004;Boushey et al 1995;Zhou et al 2001;Sutton-Tyrell et al 1997;Nygard et al 1997). Since H 2 S is highly reactive and has long been considered as toxic, its impact on various tissues is well characterised, but with recent advances in our knowledge, implicating H 2 S in Alzheimer's disease, epilepsy and stroke (Gadalla and Snyder 2010;Gupta et al 2010) as well as hypertension, future development of drugs specifically modulating H 2 S levels is likely to prove beneficial (Gupta et al 2010).…”

“…Indeed, there is a clear association between occurrence of stroke (Inoue et al 2007), myocardial infarction (Elliott 2005), heart failure (Schultz et al 2007) and kidney disease (Paoletti et al 2006), and the degree of hypertension. Despite this, the pathoaetiology of hypertension has still not been fully elucidated.…”

Contribution of Autonomic Nervous System to the Hypertension Induced by Obstructive Sleep Apnea

“…During the airflow occlusion, the resulting hypoxia and hypercapnia stimulates the carotid body chemoreceptors producing reflex ventilatory, sympathetic and hypertensive responses. Among these disturbances, the chronic intermittent hypoxia is considered the main factor for the development of the hypertension [1,19,33,41,43,51,55,56,82,83,88,93,100]. However, conclusions from studies performed in OSA patients are partial and somehow controversial, because invasive procedures are precluded because of ethical reasons in humans, and OSA patients often present concomitant morbidities (i.e.…”

The Quality of Imaging of the Carotid Body by the Standard Protocol for Computed Tomography Angiography of the Carotid Arteries

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In the late 20 th century, it was found that the basic function of the CB is chemical control of the regulation of respiratory action by means of a reflex from chemoreceptors, but it was not until the last 15 years that research has revealed another important function: the chemoreceptors present in the CB play an essential role in regulating the functions of the circulatory system [3][4][5]. Research connected with the carotid body is currently focused on establishing the significance of chronically increased CB activity in the progression of heart failure and in the genesis of hypertension [6][7][8][9].

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