Role of central hydrogen sulfide on ventilatory and cardiovascular responses to hypoxia in spontaneous hypertensive rats.

Autor: Sabino JP; Department of Morphology, Physiology and Basic Pathology, Dental School of Ribeirao Preto, University of São Paulo, 14040-904 Ribeirao Preto, SP, Brazil., Traslaviña GA; Department of Physiology, College of Medicine of Ribeirao Preto, Sao Paulo University, Brazil., Branco LG; Department of Morphology, Physiology and Basic Pathology, Dental School of Ribeirao Preto, University of São Paulo, 14040-904 Ribeirao Preto, SP, Brazil. Electronic address: branco@forp.usp.br.
Jazyk: angličtina
Zdroj: Respiratory physiology & neurobiology [Respir Physiol Neurobiol] 2016 Sep; Vol. 231, pp. 21-7. Date of Electronic Publication: 2016 May 27.
DOI: 10.1016/j.resp.2016.05.016
Abstrakt: Central hydrogen sulfide (H2S) has been reported to act as a gaseous neuromodulator involved in the ventilatory and cardiovascular control of normotensive rats, whereas no information is available in spontaneously hypertensive rats (SHR). We recorded minute ventilation (VE), mean arterial pressure (MAP) and heart rate (HR) before and after blocking of enzyme Cystathionine β-synthase (CBS) producing H2S in neural tissue by microinjection of aminooxyacetate (inhibitor of CBS) into the fourth ventricle of Wistar normotensive rats (WNR) and SHR followed by 30min of normoxia (21% inspired O2) or hypoxia (10% inspired O2) exposure. Microinjection of AOA or saline (1μL) did not change VE, MAP and HR during normoxia in both WNR and SHR. In WNR, hypoxia caused an increase in VE, HR and a decrease in MAP and these responses were unaltered by AOA. In SHR, hypoxia produced a higher increase of VE, and decrease in MAP and HR when compared to WNR, and these responses were all blunted by AOA. In conclusion, endogenous H2S plays important modulatory roles on hypoxia-induced ventilatory and cardiovascular responses, inhibiting the cardiovascular and stimulating the respiratory systems in SHR.
(Copyright © 2016 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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