Antihypertensive Actions of Vitamin B6

Vitamin B6 depletion leads to the development of hypertension in experimental animals, which is normalized within 24 hours by repletion with the vitamin.

Four mechanisms, which are not mutually exclusive, have been proposed to account for this (Dakshinamurti and Lal, 1992; Dakshinamurti, 2001):

1. Central effects on blood pressure regulation as a result of decreased synthesis of brain GABA and serotonin (5-hydroxytryptamine). Glutamate decarboxylase activity in the nervous system is especially sensitive to vitamin B6 depletion, possibly as a result of mechanism-dependent inac-tivation by transamination. Although there is no evidence that aromatic amino acid decarboxylase activity is reduced in vitamin B6 deficiency, there is reduced formation of serotonin in the central nervous system.

2. Increased sympathetic nervous system activity. There is evidence of elevated plasma concentrations of adrenaline and noradrenaline in vitamin B6-deficient animals.

3. Increased uptake of calcium by arterial smooth muscle, leading to increased muscle tone, and hence increased circulatory resistance and blood pressure. This could reflect increased sensitivity of vascular smooth muscle to calcitriol (vitamin D) action in vitamin B6 deficiency; the membrane calcium-binding protein is regulated by vitamin D, and vascular tissue has calcitriol receptors.

4. Increased end-organ responsiveness to glucocorticoids, mineralocorti-coids, and aldosterone (Section 9.3.3). Oversecretionof (andpresumably also enhanced sensitivity to) any of these hormones can result in hypertension. Vitamin B6 supplementation would be expected to reduce endorgan sensitivity to these hormones, and thus might have a hypotensive action.

A number of studies suggest that supplements of vitamin B6 may have a hypotensive action. Supplements of 300 mg of vitamin B6 per kg of body weight per day attenuated the hypertensive response of rats treated with deoxycor-ticosterone acetate (Fregly and Cade, 1995). At a more realistic level of supplementation (five times the usual amount provided in the diet), vitamin B6 prevented the development of hypertension in the Zucker (fa/fa) obese rat. Withdrawal of the vitamin supplement led to the development of hypertension (Lalet al., 1996).


A number of enzymes contain other carbonyl compounds that catalyze reactions in the same way as does pyridoxal phosphate or that catalyze redox reactions. Such compounds include pyruvate (Section 9.8.1); pyrroloquino-line quinone, which may be a dietary essential (Section 9.8.2); and a variety of other quinones that are not dietary essentials because they are formed by postsynthetic modification of precursor proteins (Section 9.8.3).

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