Sympathetic Stimulation and Hypertension in the Pyridoxine-Deficient Adult Rat

Pyridoxal phosphate is the coenzyme of various decarboxylases involved in the formation of monoamine neurotransmitters such as y-aminobutyric acid , serotonin , dopamine, and norepinephrine . Adult male Sprague-Dawley rats placed on a pyridoxine -deficient diet for 8 weeks showed significant hypertension compared with pyridoxine -supplemented controls . Hypothalamic contents of pyridoxal phosphate , y-aminobutyric acid, and serotonin in the pyridoxine - deficient rats were significantly lower than those in pyridoxine -supplemented controls . Hypertension was associated with sympathetic stimulation . Treatment of pyridoxine-deficient rats with a single dose of pyridoxine (10 mg/kg body weight) reversed the blood pressure to normal levels within 24 hours, with concomitant restorations of hypothalamic serotonin and y-aminobutyric acid as well as the return of plasma norepinephrine and epinephrine to normal levels . Also, pyridoxine treatment reversed the hypothalamic hypothyroidism observed in pyridoxine -deficient rats . These results indicate an association between pyridoxine deficiency and sympathetic stimulation leading to hypertension.

Alterations in brainstem a2 adrenoreceptor activity in pyridoxine-deficient rat model of hypertension

Moderate pyridoxine deficiency in adult male Sprague-Dawley rats results in significant hypertension, associated with a general sympathetic stimulation , including an increase in the turnover of norepinephrine in the heart. Treatment of these rats with pyridoxine reversed blood pressure to normal within 24 h. Treatment of pyridoxine-deficient rats with clonidine or x-methyl dihydroxyphenylalanine (x-methyl DOPA) also reduced the blood pressure of these animals to normal . There was also a significant increase in the Bma, of high and low affinity [3H]p-amino-clonidine binding to crude synaptosomal membrane preparations of the brain stem of deficient rats indicating chronic underexposure of)(, adrenoreceptors to endogenous norepinephrin.

Pineal indoleamine metabolism in pyridoxine-deficient rats

Pvridoxine deficiency causes physiologically significant decrease in brain serotonin (5-HT) due to decreased decarboxylation of 5- hvdroxvtrvptophan (5-HTP). We have examined the effect of pyridoxine deficiency on indoleamine metabolism in the pineal gland, a tissue with high indoleamine turnover. Adult male Sprague-Dawley rats were fed either a pyridoxine-supplemented or pyridoxinedeficient diet for 8 weeks. Pyridoxine deficiency did not alter the pattern of circadian rhythm of pineal 5-HT. 5-hvdroxvindoleacetic acid (5-HIAA), V-acetvlserotonin (NAS). and melatonin. However the levels of these compounds were significantly lower in the pineal glands of pyridoxine-deficient animals. Pineal 5-HTP levels were consistently higher in the pyridoxine-deficient animals and a conspicuous increase was noticed at 22.00 h. Increase in pineal NAS and melatonin levels caused by isoproterenol (5 mg kg at 17.00 h) were significantly lower (P < 0.05) in the pyridoxine-deficient animals. Treatment of pyridoxine-deficient rats with pvridoxine restored the levels of pineal 5-HT, 5-HIAA. NAS. and melatonin to values seen in pyridoxine-supplemented control animals. These results suggest that 5-HT availability could be an important factor in the regulation of the synthesis of pineal NAS and melatonin.