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Do changes in the coupling between respiratory and sympathetic activities contribute to neurogenic hypertension?
Author(s) -
Zoccal Daniel B,
Paton Julian FR,
Machado Benedito H
Publication year - 2009
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2009.05202.x
Subject(s) - respiratory system , sympathetic nervous system , hypoxia (environmental) , medicine , neuroscience , autonomic nervous system , mechanism (biology) , rostral ventrolateral medulla , respiration , central nervous system , chemistry , biology , heart rate , blood pressure , medulla oblongata , anatomy , oxygen , philosophy , organic chemistry , epistemology
Summary1 It is well known that respiration markedly modulates the sympathetic nervous system. Interactions between pontine and medullary neurons involved in the control of sympathetic and respiratory functions are the main mechanism underlying the respiratory related oscillations in sympathetic nerve activity. 2 Recently, in rats treated with chronic intermittent hypoxia, we demonstrated that alterations in respiratory pattern may drive increased sympathetic outflow and hence the development of systemic hypertension. These experiments, performed in the in situ working heart–brain stem preparation, raise the possibility that enhanced central coupling between respiratory and sympathetic activities could be a potential mechanism underpinning the development and/or the maintenance of neurogenic hypertension. 3 In the present review, we discuss the neural basis of the enhanced entrainment between respiratory and sympathetic neurons in the brain stem that can be induced by chronic intermittent hypoxia and the possible implications of these mechanisms in the genesis of sympathetic overactivity and, consequently, hypertension.