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低钙诱导的收缩压升高与维生素B6之间的关系。

The relationship between low-calcium-induced increase in systolic blood pressure and vitamin B6.

作者信息

Lal K J, Dakshinamurti K

机构信息

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

出版信息

J Hypertens. 1995 Mar;13(3):327-32.

PMID:7622854
Abstract

OBJECTIVE

To investigate the relationship between the increase in systolic blood pressure caused by a low-calcium (0.1%) diet and the vitamin B6 status in the rat.

METHODS

Male Sprague-Dawley rats fed a vitamin B6-deficient diet did not show any change in systolic blood pressure (SBP) for the first 4 weeks (prehypertensive phase), but from week 5 there was an increase in SBP lasting until week 10 (hypertensive phase). SBP declined to below normal levels in most rats from week 12 on the vitamin B6-deficient diet (posthypertensive phase). The effect of altering the level of calcium in the diet at different phases of vitamin B6 deficiency was studied. In another experiment the effect on the change in blood pressure induced by the low-calcium diet of increasing the dietary vitamin B6 level to 2.5-, 5- or 10-fold the normal intake was studied.

RESULTS

Lowering dietary calcium caused a significant increase in SBP in rats on the vitamin B6-sufficient diet. This occurred during weeks 3 and 4 on the low-calcium diet. Low levels of calcium on the diet potentiated the hypertension induced by the vitamin B6-deficient diet when both deficiencies were present from the beginning of the experiment. Feeding a low-calcium diet during the hypertensive or posthypertensive phase failed to raise the SBP in these rats. Normalizing the vitamin B6 status of posthypertensive vitamin B6-deficient rats restored the ability of low dietary calcium to increase SBP in these rats. Increasing dietary levels of vitamin B6 by itself reduced SBP in normal rats, and attenuated the increase in SBP induced by the low-calcium diet.

CONCLUSIONS

Dietary vitamin B6 deficiency and low calcium in the diet seem to share the mechanisms increasing SBP.

摘要

目的

研究低钙(0.1%)饮食导致的收缩压升高与大鼠维生素B6状态之间的关系。

方法

喂食维生素B6缺乏饮食的雄性Sprague-Dawley大鼠在最初4周(高血压前期)收缩压(SBP)未出现任何变化,但从第5周开始SBP升高,持续至第10周(高血压期)。在维生素B6缺乏饮食的情况下,大多数大鼠从第12周开始SBP降至正常水平以下(高血压后期)。研究了在维生素B6缺乏的不同阶段改变饮食中钙水平的影响。在另一项实验中,研究了将饮食中维生素B6水平提高至正常摄入量的2.5倍、5倍或10倍对低钙饮食诱导的血压变化的影响。

结果

降低饮食中的钙会导致喂食维生素B6充足饮食的大鼠SBP显著升高。这发生在低钙饮食的第3周和第4周。当从实验开始就同时存在两种缺乏时,饮食中低水平的钙会增强维生素B6缺乏饮食诱导的高血压。在高血压期或高血压后期喂食低钙饮食未能提高这些大鼠的SBP。使高血压后期维生素B6缺乏大鼠的维生素B6状态正常化可恢复低饮食钙增加这些大鼠SBP的能力。单独提高饮食中维生素B6的水平可降低正常大鼠的SBP,并减弱低钙饮食诱导的SBP升高。

结论

饮食中维生素B6缺乏和低钙似乎具有共同的增加SBP的机制。

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