Abstract-We studied the effect of oral cholecalciferol treatment on the endothelium-dependent vascular relaxation and hyperpolarization induced by acetylcholine (ACh), which is impaired in spontaneously hypertensive rats (SHR). Adult female SHR and normotensive Wistar-Kyoto rat (WKY) controls received 125 g of cholecalciferol per kilogram body weight per day for 6 weeks. The responses to ACh of the isolated mesenteric vascular bed and mesenteric artery rings were measured, as well as the smooth muscle cell membrane potential. After cholecalciferol treatment, the systolic blood pressure and basal perfusion pressure of the mesenteric vascular bed of the SHR fell to control levels. The relaxant and hyperpolarizing effects of ACh, which are reduced in SHR, were also brought to control levels after cholecalciferol treatment. These effects of ACh were inhibited by N -nitro-L-arginine in SHR and by apamin in WKY. After cholecalciferol treatment, SHR hyperpolarizing responses showed the same inhibition pattern as those of WKY. This indicates that, after cholecalciferol treatment, SHR vascular mesenteric preparation responses to ACh are mediated by endothelium-derived hyperpolarizing factor, which induces activation of Ca 2ϩ -dependent K ϩ channels, as in WKY. In untreated SHR, the ACh-mediated response is entirely due to ACh acting via the release of nitric oxide.

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 71 body weight per day orally caused signi®cant reductions of systolic blood pressure and of the resting perfusion pressure of the mesenteric vascular bed at constant¯ow. 2 In addition, the treated animals presented a normalization of the maximum vasoconstriction response to noradrenaline and a reduction of the maximum eect of the adrenaline concentrationresponse curves. This latter eect probably was due to recovery of the impaired Ca 2+ -dependent K + channels coupled to a 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 a 2 -adrenergic agonists, which were depressed in untreated SHR. 4 In mesenteric rings with endothelium, a 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 eect was NO, while in NWR it was the endothelium-derived hyperpolarizing factor (EDHF). After cholecalciferol treatment, the hyperpolarization induced by a 2 -adrenergic agonists in SHR smooth muscle cells was mediated by EDHF, as in NWR. 5 Our results indicate that the hypotensive eect 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.

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No Brasil, devido às mudanças nos perfis demográfico, epidemiológico e nutricional da população e ao controle conseguido em um número de enfermidades transmissíveis, vêm observando-se, nas últimas décadas, uma inversão do perfil epidemiológico com redução das doenças infecciosas e o aumento significativo da prevalência das doenças crônicas não transmissíveis (DCNTs). Essa mudança justifica o estudo dos fatores de risco e determinantes sociais das doenças crônico-degenerativas no país. O presente trabalho teve por objetivo conhecer a prevalência da exposição da população aos principais fatores de risco para o desenvolvimento de DCNTs no Brasil. Foi realizada uma revisão sistemática dos artigos publicados na literatura científica, a partir das bases de dados on-line Lilacs e Medline, entre 2003 e 2008, em português. As prevalências variaram conforme os critérios utilizados e as características das populações estudadas, sendo obtidos os seguintes valores mínimo e máximo para cada um dos fatores de risco estudados: tabagismo 8,7% a 28,8%, uso abusivo de álcool 0,1% a 37,7%, excesso de peso 1,5% a 49,0%, obesidade 9,4% a 17,6%, sedentarismo 20,1% a 43,1%, hipertensão arterial 5,3% a 34,0%, diabetes mellitus 2,7% a 7,8%. A variação no grau de exposição da população aos fatores de risco presentes nos diversos estudos aponta para a necessidade de padronização dos instrumentos de medida, a fim de que os resultados obtidos nas diferentes localidades possam ser comparados. Além disso, as altas prevalências observadas em algumas áreas indicam a necessidade de intervenções imediatas por meio da implementação de estratégias de prevenção e promoção da saúde dirigidas à redução da exposição da população brasileira aos fatores associados ao risco de desenvolvimento das DCNTs.