The Nervous Mechanism of Sympathetic over Activity Induced by Chronic Intermittent HypoxiaQi An and En-Sheng Ji*
Department of Physiology, School of Basic Medicine, Hebei University of Traditional Chinese Medicine, China
- *Corresponding Author:
- En-Sheng Ji
Department of Physiology, School of Basic Medicine
Hebei University of Traditional Chinese Medicine, 326
Xinshi South Road, Shijiazhuang 050091, Hebei, P.R. China
Tel: +86 311 86265107
Fax: +86 311 86265174
E-mail: [email protected]
Received date: December 27, 2013; Accepted date: January 27, 2014; Published date: January 30, 2014
Citation: An Q, Ji ES (2014) The Nervous Mechanism of Sympathetic over Activity Induced by Chronic Intermittent Hypoxia. J Pulm Respir Med 4:170. doi:10.4172/2161-105X.1000170
Copyright: © 2014 An Q, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Hypertension is concerned to be a common complication in Chronic Intermittent Hypoxia (CIH) conditions which mimic the state of Obstructive Sleep Apnoea (OSA) in clinic. Sympathoexcitation is a crucial origin in the process of high blood pressure and the mechanisms involved in the sympathoexicitatory changes after CIH exposure are complex referring to chemoreflex, baroreflex, neurotransmitters, and central nuclei and so on. In this review we predominantly expound the effect of CIH-induced potentiated Carotid Body (CB) chemoreceptor sensitivity to hypoxia stimulation which results in the enhancement of RSNA and Endothelin (ET) is mentioned due to its expression in CB and the fact that ET is thought to be a significant chemoreceptor-excitatory transmitter. Previously studies have shown expression of ET and ET receptors in the CB chemoreceptor glomus cells and vessel system, and CIH obviously increased the expression which indicated a possible effect of ET to the potentiated ventilatory and cardiovascular responses to acute hypoxia probably via increased inward Ca2+ currents, inflammatory response or Acid-Sensitive Ion Channels (ASICs) in chemoafferent neurons in the petrosal ganglion. However we also display the effect of enhanced central respiratory-sympathetic coupling which also participated in the increase in sympathetic activity. The other mechanism introduced in this review is the role of the Nucleus Tractus Solitarius (NTS) after CIH exposure. Neurotransmitters like ET and Glutamate act on the cerebroventricle and the NTS elicit significantly increase of RSNA in CIH group. The sympathetic nerve originated site Rostral Ventrolateral Medulla (RVLM) also makes adaptive changes after CIH to copes the hypoxia stimulation and induces RSNA responses. At last we raise the phenomenon that depressed baroreflex sensitivity emerged after a long time CIH exposure and is involved in the process of sustained high blood pressure.