Enhanced sympathetic neurotransduction in the superior mesenteric artery in a rat model of heart failure: role of noradrenaline and ATP

Autor(es)

Blanco-Rivero, Javier ^{[1, 2, 3, 4]} ; Couto, Gisele K. ^[4] ; Paula, Suliana M. ^[4] ; Fontes, Milene T. ^[4] ; Rossoni, V, Luciana

Afiliação do(s) autor(es)

^[1] Univ Autonoma Madrid, Sch Med, Dept Physiol, Madrid - Spain

^[2] Ctr Biomed Res Network Cardiovasc Dis CiberCV, Madrid - Spain

^[3] Res Inst Univ Hosp Paz IdiPaz, Madrid - Spain

^[4] V, Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY; v. 320, n. 2, p. H563-H574, FEB 2021.
• Citações Web of Science: 0

Resumo

Heart failure (HF) is associated with neurohumoral activation, which in turn leads to an increased peripheral resistance. In mesenteric vasculature, perivascular innervation plays relevant role maintaining vascular tonus and resistance. Therefore, we aimed to determine the possible alterations in superior mesenteric artery (SMA) perivascular innervation function in HF rats. HF was induced by coronary artery occlusion in male Wistar rats, and sham-operated (SO) rats were used as controls. After 12 wk, a greater vasoconstrictor response to electrical field stimulation (EFS) was observed in endothelium-intact and endothelium-denuded SMA of HF rats. Alpha-adrenoceptor antagonist phentolamine diminished this response in a higher magnitude in HF than in SO animals. However, the noradrenaline (NA) reuptake inhibitor desipramine increased EFS-induced vasoconstriction more in segments from HF rats. Besides, EFS-induced NA release was greater in HF animals, due to a higher tyrosine hydroxylase expression and activity. P2 purinoceptor antagonist suramin reduced EFS-induced vasoconstriction only in segments from SO rats, and adenosine 5'-triphosphate (ATP) release was lower in HF than in SO. Moreover, nitric oxide (NO) synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) enhanced EFS-induced vasoconstriction in a similar extent in both groups. HF was not associated with changes in EFS-induced NO release or the vasodilator response to NO donor sodium nitroprusside. In conclusion, HF postmyocardial infarction enhanced noradrenergic function and diminished purinergic cotransmission in SMA and did not change nitrergic innervation. The net effect was an increased sympathetic participation on the EFS-induced vasoconstriction that could help to understand the neurotransduction involved on the control of vascular tonus in HF. NEW \& NOTEWORTHY This study reinforces the pivotal role of noradrenergic innervation in the regulation of mesenteric vascular tone in a rat model of heart failure. Moreover, our results highlight the counteracting role of ATP and NA reuptake, and help to understand the signaling pathways involved on the control of vascular tonus and resistance in heart failure postmyocardial infarction. (AU)

• Processo FAPESP: 10/50048-1 - Bases celulares e funcionais do exercício físico na doença cardiovascular
• Beneficiário: Carlos Eduardo Negrão
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 14/20303-0 - Avaliação da influência do tecido adiposo perivascular (PVAT) na reatividade vascular da aorta de ratos infartados submetidos ao treinamento físico aeróbio e resistido
• Beneficiário: Milene Tavares Fontes
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 14/22335-7 - Avaliação da inervação perivascular em artérias de ratos pós-infarto do miocárdio: efeito do treinamento físico aeróbio
• Beneficiário: Luciana Venturini Rossoni
• Modalidade de apoio: Auxílio à Pesquisa - Pesquisador Visitante - Internacional