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消旋-α-生育酚烟酸酯对大鼠的降压作用

Antihypertensive action of d,l-alpha-tocopheryl nicotinate in rats.

作者信息

Igarashi T, Nakajima Y, Kobayashi M, Ohtake S

出版信息

J Nutr Sci Vitaminol (Tokyo). 1979;25(3):159-73. doi: 10.3177/jnsv.25.159.

DOI:10.3177/jnsv.25.159
PMID:501448
Abstract

The effects of d,l-alpha-tocopheryl nicotinate (EN) on model hypertension in rats were studied in comparison with d,l-alpha-tocopheryl acetate (EA). The progress of hypertension in young SHR during the 9th to 15th weeks after birth was markedly accelerated by replacing their driking water with 1% saline. The highly-developed hypertension in old SHR (9 months of age) was further advanced by salt-loading. Oral administration of 20 or 100 mg/kg of EN or 88 mg/kg of EA, once a day, delayed the progress of hypertension in young SHR and reduced advanced hypertension in old SHR. An antihypertensive effect of tocopheryl esters was also found in DOCA-salt hypertensive rats. The treatment with EN or EA definitely reduced the incidence of pathological changes accompanying model hypertension such as suppressed weight gain, pulmonary edema, myocardial fibrosis, cerebral hemorrhage and protected the animals from death. In antihypertensive effect, EN was about 5 times more active than EA in molecular base, and the effects of EN protecting from pathological changes associated with model hypertension were more definite than those of EA. The treatment with EN or EA reduced water and sodium retention in the DOCA-salt hypertensive animals. This fact may suggest the implication of a mechanism through electrolyte metabolism in the antihypertensive action of these tocopheryl esters.

摘要

研究了d,l-α-生育酚烟酸酯(EN)与d,l-α-生育酚乙酸酯(EA)相比对大鼠模型高血压的影响。用1%盐水替代幼龄自发性高血压大鼠(SHR)出生后第9至15周的饮用水,显著加速了高血压的进展。给老年SHR(9月龄)高盐负荷可使已高度发展的高血压进一步加重。每天口服20或100mg/kg的EN或88mg/kg的EA可延缓幼龄SHR高血压的进展,并降低老年SHR的重度高血压。在去氧皮质酮-盐性高血压大鼠中也发现了生育酚酯的降压作用。用EN或EA治疗可明确降低模型高血压伴随的病理变化发生率,如体重增加受抑、肺水肿、心肌纤维化、脑出血,并保护动物免于死亡。在降压作用方面,在分子基础上EN的活性比EA高约5倍,且EN预防与模型高血压相关病理变化的作用比EA更确切。用EN或EA治疗可减少去氧皮质酮-盐性高血压动物的水钠潴留。这一事实可能提示这些生育酚酯的降压作用中存在通过电解质代谢的机制。

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