Endogenous hydrogen sulfide in the rostral ventrolateral medulla/Botzinger complex downregulates ventilatory responses to hypoxia

Autor(es)

Donatti, Alberto F. ^[1] ; Soriano, Renato N. ^[1] ; Sabino, Joao P. ^[1] ; Branco, Luiz G. S. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Dent Sch Ribeirao Preto, Dept Morphol Physiol & Basic Pathol, BR-14040904 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Respiratory Physiology & Neurobiology; v. 200, p. 97-104, AUG 15 2014.
• Citações Web of Science: 7

Resumo

Hydrogen sulfide (H2S) is now recognized as a new gaseous transmitter involved in several brain-mediated responses. The rostral ventrolateral medulla (RVLM)/Botzinger complex is a region in the brainstem that is involved in cardiovascular and respiratory functions. Recently, it has been shown that exogenous H2S in the RVLM modulates autonomic function and thus blood pressure. In the present study, we investigated whether H2S, endogenously produced in the RVLM/Botzinger complex, plays a role in the control of hypoxia-induced hyperventilation. Ventilation (V-E) was measured before and after bilateral microinjection of Na2S (H2S donor, 0.04, 1 and 2 pmol/100 nl) or aminooxyacetate (AOA, 0.2, 1 and 2 pmol/100 nl, a cystathionine beta-synthase, CBS, inhibitor) into the RVLM/Botzinger complex followed by a 60-min period of hypoxia (7% inspired O-2) or normoxia exposure. Control rats received microinjection of vehicle. Microinjection of vehicle, AOA or Na2S did not change V-E in normoxic conditions. Exposure to hypoxia evoked a typical increase in V-E. Microinjection of Na2S (2 pmol) followed by hypoxia exposure attenuated the hyperventilation. Conversely, microinjection of AOA (2 pmol) into the RVLM/Botzinger complex caused an increase in the hypoxia-induced hyperventilation. Thus, endogenous H2S in the RVLM/Botzinger complex seems to play no role in the maintenance of basal pulmonary ventilation during normoxia whereas during hypoxia H2S has a downmodulatory function. Homogenates of RVLM/Botzinger complex of animals previously exposed to hypoxia for 60 min exhibited a decreased rate of H2S production. Our data are consistent with the notion that the gaseous messenger H2S synthesis is downregulated in the RVLM/Botzinger complex during hypoxia favoring hyperventilation. (C) 2014 Elsevier B.V. All rights reserved. (AU)

• Processo FAPESP: 12/01417-0 - Participação do sulfeto de hidrogênio (H2S) no bulbo ventrolateral rostral na modulação da resposta ventilatória à hipóxia
• Beneficiário: Alberto Ferreira Donatti
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado