Differential regulation of atrial contraction by P1 and P2 purinoceptors in normotensive and spontaneously hypertensive rats

Nenhuma Miniatura disponível
Data
2014-03-01
Autores
Dantas Rodrigues, Juliano Quintella [UNIFESP]
Silva, Edilson Dantas da [UNIFESP]
Galvao, Kleber de Magalhaes [UNIFESP]
Miranda-Ferreira, Regiane [UNIFESP]
Caricati-Neto, Afonso [UNIFESP]
Jurkiewicz, Neide Hyppolito [UNIFESP]
Garcia, Antonio G.
Jurkiewicz, Aron [UNIFESP]
Orientadores
Tipo
Artigo
Título da Revista
ISSN da Revista
Título de Volume
Resumo
In the normotensive rat atrium, adenosine-5'-triphosphate and uridine-5'-triphosphate exert a biphasic effect consisting of an initial negative inotropic effect (NIE) followed by a subsequent positive inotropic effect (PIE). We comparatively studied these responses in normotensive Wistar rats (NWRs) and spontaneously hypertensive rats (SHRs). Compared with NWRs, the NIE responses in the atria were lower and the PIE responses were higher in SHRs. the P1 purinoceptor antagonist, D 8-cyclopentyl-1,3- dipropylxanthine, partially blocked the NIE responses of both ATP and UTP and mildly enhanced the PIE responses in both NWRs and SHRs. Furthermore, the P2 purinoceptor blockers suramin and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid tetrasodium salt induced a pronounced block of the PIE responses in both atria types. the PIE responses to ATP were inhibited more efficiently by nifedipine. These responses were depressed by ryanodine and, to a lesser extent, carbonyl cyanide 3-chlorophenylhydrazone in SHR atria compared with NWR atria. the higher responses in SHR rats suggest the existence of an augmented endoplasmic reticulum Ca2+ store and faster mitochondrial Ca2+ cycling in SHR atria compared with NWR atria. These data support the hypothesis that a dysfunction of purinergic neurotransmission and enhanced sympathetic activity are contributing factors in the pathogenesis of hypertension.
Descrição
Citação
Hypertension Research. London: Nature Publishing Group, v. 37, n. 3, p. 210-219, 2014.
Coleções