Resenha
Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympathetic nervous system
Registro en:
Breathing, Emotion And Evolution. Amsterdam: Elsevier Science Bv, v. 212, p. 1-23, 2014.
0079-6123
10.1016/B978-0-444-63488-7.00001-X
WOS:000349339500002
1958567557189244
Autor
Molkov, Yaroslav I.
Zoccal, Daniel Breseghello [UNESP]
Baekey, David M.
Abdala, Ana Paula L.
Machado, Benedito Honório
Dick, Thomas E.
Paton, Julian F. R.
Rybak, Ilya A.
Resumen
Respiratory modulation seen in the sympathetic nerve activity (SNA) implies that the respiratory and sympathetic networks interact. During hypertension elicited by chronic intermittent hypoxia (CIH), the SNA displays an enhanced respiratory modulation reflecting strengthened interactions between the networks. In this chapter, we review a series of experimental and modeling studies that help elucidate possible mechanisms of sympatho-respiratory coupling. We conclude that this coupling significantly contributes to both the sympathetic baroreflex and the augmented sympathetic activity after exposure to CIH. This conclusion is based on the following findings. (1) Baroreceptor activation results in perturbation of the respiratory pattern via transient activation of postinspiratory neurons in the Botzinger complex (BotC). The same BotC neurons are involved in the respiratory modulation of SNA, and hence provide an additional pathway for the sympathetic baroreflex. (2) Under hypercapnia, phasic activation of abdominal motor nerves (AbN) is accompanied by synchronous discharges in SNA due to the common source of this rhythmic activity in the retrotrapezoid nucleus (RTN). CIH conditioning increases the CO2 sensitivity of central chemoreceptors in the RTN which results in the emergence of AbN and SNA discharges under normocapnic conditions similar to those observed during hypercapnia in naive animals. Thus, respiratory-sympathetic interactions play an important role in defining sympathetic output and significantly contribute to the sympathetic activity and hypertension under certain physiological or pathophysiological conditions, and the theoretical framework presented may be instrumental in understanding of malfunctioning control of sympathetic activity in a variety of disease states. Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Indiana University-Purdue University, Department of Mathematical Sciences University of Florida, Department of Physiological Sciences University of Bristol, School of Physiology and Pharmacology, Bristol Heart Institute Universidade de São Paulo, Departmento of Fisiologia, Faculdade de Medicina de Ribeirão Preto Case Western Reserve University, Departments of Medicine and Neurosciences Drexel University College of Medicine, Department of Neurobiology and Anatomy Universidade Estadual Paulista, Departamento de Fisiologia e Patologia, Faculdade de Odontologia de Araraquara