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      Effect of bilateral carotid body resection on the counterregulatory response to hypoglycaemia in humans : Carotid body resection and hypoglycaemia

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          Most cited references 23

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          Carotid Body Denervation Prevents the Development of Insulin Resistance and Hypertension Induced by Hypercaloric Diets

          Increased sympathetic activity is a well-known pathophysiological mechanism in insulin resistance (IR) and hypertension (HT). The carotid bodies (CB) are peripheral chemoreceptors that classically respond to hypoxia by increasing chemosensory activity in the carotid sinus nerve (CSN), causing hyperventilation and activation of the sympathoadrenal system. Besides its role in the control of ventilation, the CB has been proposed as a glucose sensor implicated in the control of energy homeostasis. However, to date no studies have anticipated its role in the development of IR. Herein, we propose that CB overstimulation is involved in the etiology of IR and HT, core metabolic and hemodynamic disturbances of highly prevalent diseases like the metabolic syndrome, type 2 diabetes, and obstructive sleep apnoea. We demonstrate that CB activity is increased in IR animal models and that CSN resection prevents CB overactivation and diet-induced IR and HT. Moreover, we show that insulin triggers CB, highlighting a new role for hyperinsulinemia as a stimulus for CB overactivation. We propose that CB is implicated in the pathogenesis of metabolic and hemodynamic disturbances through sympathoadrenal overactivation and may represent a novel therapeutic target in these diseases.
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            Low glucose-sensing cells in the carotid body.

            Decreased plasma glucose concentration elicits a complex neuroendocrine response that prevents or rapidly corrects hypoglycemia as required to preserve brain function; however, where and how low glucose is sensed is unknown. Here we show that low glucose increases secretion from glomus cells in the carotid bodies, sensory organs whose stimulation by hypoxia produces sympathetic activation, by a process that depends on extracellular Ca2+ influx and is paralleled by inhibition of voltage-gated K+ channels. We propose a new glucose-sensing role for the carotid body glomus cell that serves to integrate information about blood glucose and O2 levels and to activate counterregulatory responses.
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              Denervation of carotid baro- and chemoreceptors in humans.

              Experimental denervation in animals has shown that carotid baro- and chemoreceptors play an eminent role in maintaining blood pressure and blood gas homeostasis. Denervation of carotid sinus baro- and chemoreceptors in humans may occur as a complication of invasive interventions on the neck or after experimental surgical treatment in asthma. In this topical review, the short- and long-term effects of carotid baro- and chemoreceptor denervation on the control of circulation and ventilation in humans are discussed. Carotid baroreceptor denervation in humans causes a persistent decrease in vagal and sympathetic baroreflex sensitivity and an increase in blood pressure variability; however, carotid denervation does not lead to chronic hypertension. Therefore, although carotid baroreceptors contribute to short-term blood pressure control, other receptors are able to maintain normal chronic blood pressure levels in the absence of carotid baroreceptors. Conversely, carotid chemoreceptor denervation leads to permanent abolition of normocapnic ventilatory responses to hypoxia and reduced ventilatory responses to hypercapnia.
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                Author and article information

                Journal
                Experimental Physiology
                Exp Physiol
                Wiley
                09580670
                January 01 2015
                January 01 2015
                December 31 2014
                : 100
                : 1
                : 69-78
                Affiliations
                [1 ]Department of Physiology; Michigan State University; East Lansing MI USA
                [2 ]Department of Anesthesiology; Mayo Clinic; Rochester MN USA
                [3 ]Department of Endocrinology; Mayo Clinic; Rochester MN USA
                Article
                10.1113/expphysiol.2014.083154
                © 2014
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