Viswanathan,M; Paulose,C S; Lal,K J; Sharma,S K; Dakshinamurti,K(Department of Biotechnology, November 27, 1989)
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Abstract:
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.
Paulose,C S; Dakshinamurti,K; Subah,Packer; Newman,L Stephens(Department of Biotechnology, 1986)
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Abstract:
Pyridoxal phosphate (PLP) is the coenzyme of various decarboxylases involved in the
formation of monoamine urotransmitters such as y-aminobulyric acid (GAE3A),
serotonin (5-HT) and dopamine. 1-lowever; in the pyridoxine-deficient rats GABA and
5-HT are decreased in various brain areas including the hypothalamus, with no change
in the catecholamine levels. Serotonin and GABA are known to be involved in blood
pressure control mechanisms. In this study adult Sprague-Dawley rats placed on a
pyridoxine-deficient diet for 8 weeks showed significant hypertension compared with
pyridoxine-supplemented controls. This was associated with a general sympathetic
stimulation. Treatment of deficient rats with a single dose of pyridoxine (10 mg/kg body
weight) reversed the blood pressure to normal levels within 24 h, with concomitant
restoration of hypothalamic 5-HT and GABA, as well as the return of plasma
norepinephrine to nornr;l levels. The results indicate that there is a cause-and-effect
relationship between pyridoxine deficiency and hypertension.
Viswanathan,M; Siow,Y L; Paulose,C S; Dakshinamurti,K(Department of Biotechnology, May 24, 1988)
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Abstract:
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.