Recovery of impaired K+ channels in mesenteric arteries from spontaneously hypertensive rats by prolonged treatment with cholecalciferol

Recovery of impaired K+ channels in mesenteric arteries from spontaneously hypertensive rats by prolonged treatment with cholecalciferol

Autor Borges, Antonio Carlos R Google Scholar
Feres, Teresa Google Scholar
Vianna, Lucia M. Google Scholar
Paiva, Therezinha B. Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Resumo 1 the mechanism responsible for blood pressure reduction in spontaneously hypertensive rats (SHR) after prolonged cholecalciferol treatment was studied. Two-week treatment of SHR with 0.125 mg cholecalciferol kg(-1) body weight per day orally caused significant reductions of systolic blood pressure and of the resting perfusion pressure of the mesenteric vascular bed at constant flow.2 in addition, the treated animals presented a normalization of the maximum vasoconstriction response to noradrenaline and a reduction of the maximum effect of the adrenaline concentration-response curves. This latter effect probably was due to recovery of the impaired Ca2+-dependent K+ channels coupled to alpha(2)-adrenoceptors since it was prevented by apamin.3 the treatment with cholecalciferol also normalized the smooth muscle cell membrane potential of de-endothelialized mesenteric arteries of SHR and their hyperpolarizing responses to alpha(2)-adrenergic agonists, which were depressed in untreated SHR.4 in mesenteric rings with endothelium, alpha(2)-adrenergic agonists caused similar hyperpolarizing responses in the SHR and in normotensive Wistar (NWR) and Wistar Kyoto (WKY). in non cholecalciferol-treated SHR the hyperpolarizing mediator involved in this effect was NO, while in NWR it was the endothelium-derived hyperpolarizing factor (EDI-IF). After cholecalciferol treatment, the hyperpolarization induced by alpha(2)-adrenergic agonists in SHR smooth muscle cells was mediated by EDHF, as in NWR.5 Our results indicate that the hypotensive effect of cholecalciferol in the SHR is probably due to the normalization of vascular reactivity, by restoring the functioning of apamin- and ATP-sensitive K+ channels located in the vascular smooth muscle cell membrane, which are impaired in the SHR.
Palavra-chave SHR
mesenteric arteries
membrane potential
alpha-2 adrenoceptors
K+ channels
Idioma Inglês
Data de publicação 1999-06-01
Publicado em British Journal of Pharmacology. Basingstoke: Stockton Press, v. 127, n. 3, p. 772-778, 1999.
ISSN 0007-1188 (Sherpa/Romeo, fator de impacto)
Publicador Stockton Press
Extensão 772-778
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000080796000023
Endereço permanente

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