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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Sabino, Joao Paulo J. [1] ; Soriano, Renato N. [2] ; Santos, Bruna M. [3] ; Donatti, Alberto F. [4] ; Fernandez, Rodrigo R. [3] ; da Silva, Glauber S. F. [5] ; Branco, Luiz G. S. [3]
Total Authors: 7
[1] Univ Fed Piaui, Dept Biophys & Physiol, Teresina, PI - Brazil
[2] Univ Fed Juiz de Fora, Dept Basic Life Sci, Div Physiol & Biophys, Governador Valadares, MG - Brazil
[3] Univ Sao Paulo, Dent Sch Ribeirao Preto, Dept Morphol Physiol & Basic Pathol, Ribeirao Preto, SP - Brazil
[4] Fac Estacio Sa Campo Grande, Campo Grande, MS - Brazil
[5] Univ Fed Minas Gerais, Inst Biol Sci, Dept Physiol & Biophys, Belo Horizonte, MG - Brazil
Total Affiliations: 5
Document type: Journal article
Source: Respiratory Physiology & Neurobiology; v. 263, p. 38-46, MAY 2019.
Web of Science Citations: 0

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 beta-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 (V-E), and deep body temperature (Tb) of SHR and (normotensive) Wistar Kyoto (WKY) rats before and after microinjection of AOA (9 nmol/mu L) 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 V-E, 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 V-E, 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 V-E, 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. (AU)

FAPESP's process: 11/14779-4 - Effect of hydrogen sulfide (H2S) in the commissural NTS on the ventilatory and hemodynamic response to hypoxia and hypercapnia in normotensive and hypertensive animals
Grantee:João Paulo Jacob Sabino
Support type: Scholarships in Brazil - Post-Doctorate