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Respir Physiol Neurobiol. 2019 Mar 1;263:38-46. doi: 10.1016/j.resp.2019.03.001. [Epub ahead of print]

Central administration of aminooxyacetate, an inhibitor of H2S production, affects thermoregulatory but not cardiovascular and ventilatory responses to hypercapnia in spontaneously hypertensive rats.

Author information

1
Department of Biophysics and Physiology, Federal University of Piaui, Teresina, PI, Brazil.
2
Division of Physiology and Biophysics, Department of Basic Life Sciences, Federal University of Juiz de Fora, Governador Valadares, MG, Brazil.
3
Department of Morphology, Physiology and Basic Pathology, Dental School of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, SP, Brazil.
4
Faculdade Estacio de Sa de Campo Grande, Campo Grande, MS, Brazil.
5
Federal University of Minas Gerais, Institute of Biological Science, Department of Physiology and Biophysics, Belo Horizonte, MG, Brazil.
6
Department of Morphology, Physiology and Basic Pathology, Dental School of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, SP, Brazil. Electronic address: branco@forp.usp.br.

Abstract

Hydrogen sulfide (H2S) is classically known for its toxic effects. More recently H2S has been documented as a neuromodulator. Here we investigated the central effects of aminooxyacetate (AOA; inhibitor of the H2S-synthesizing enzyme cystathionine β-synthase, CBS) on cardiovascular, respiratory and thermoregulatory responses to hypercapnia in spontaneously hypertensive rats (SHR). To attain this goal we measured mean arterial pressure (MAP), heart rate (HR), ventilation (VE), and deep body temperature (Tb) of SHR and (normotensive) Wistar Kyoto (WKY) rats before and after microinjection of AOA (9 nmol/μL) or saline into the fourth ventricle immediately followed by 30-min hypercapnia exposure (7% inspired CO2). In saline-treated WKY rats, hypercapnia caused an increase in MAP accompanied by bradycardia, an increase in VE, and a drop in Tb. In AOA-treated WKY rats exposed to hypercapnia, the drug did not affect the increased MAP, potentiated the bradycardic response, attenuated the increased VE, and potentiated the drop in Tb. In saline-treated SHR, in comparison to the saline-treated WKY rats, hypercapnia elicited a minor, shorter-lasting increase in MAP with no changes in HR, evoked a greater increase in VE, and did not induce a drop in Tb. In AOA-treated SHR exposed to hypercapnia, the drug did not change the hypercapnia-induced cardiovascular and ventilatory responses while permitted a drop in Tb. Our findings indicate that AOA, an inhibitor of H2S production, modulates cardiorespiratory and thermoregulatory responses to hypercapnia in normotensive rats, whereas hypertension development in SHR is accompanied by suppression of the AOA effect on the cardiovascular and respiratory responses.

KEYWORDS:

Arterial blood pressure; Deep body temperature; Fourth ventricle; Heart rate; Pulmonary ventilation

PMID:
30831241
DOI:
10.1016/j.resp.2019.03.001

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