Lungen- und Atemwegsmedizin

The Nervous Mechanism of Sympathetic over Activity Induced by Chronic Intermittent Hypoxia

Abstract

Qi An and En-Sheng Ji

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.