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Biomedical subjects

K Dakshinamurti

Publications and source records attributed to K Dakshinamurti.

At least 19 recordsLinked to original sources
PubMed1993

Calcium channels in vitamin B6 deficiency-induced hypertension.

OBJECTIVE: To compare the acute hypotensive effects of various calcium channel modulators in vitamin B6-deficient hypertensive (B6DHT) rats. METHODS: Adult male Sprague-Dawley rats were fed a vitamin B6-deficient diet for 7-10 weeks, during which systolic blood pressure (SBP) was measured in the B6DHT and control rats, using tail-cuff plethysmography. The effects of the calcium antagonists nifedipine, verapamil, diltiazem and (-)-202-791 on SBP were determined in conscious B6DHT rats. The effect of the calcium agonist BAY K 8644 on the SBP of rats fed various levels of pyridoxine was also determined. RESULTS: All of the calcium antagonists used were effective in lowering the SBP of the B6DHT rats with the rank order of potency: nifedipine > (-)-202-791 > (+/-)-verapamil > diltiazem. BAY K 8644 elevated the SBP of older rats fed a normal commercially available diet, but had no effect when the vitamin B6 content of their diet was increased or removed for a short period. CONCLUSION: Calcium channel function appears to be related to vitamin B6 status in the rat.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Determination of vitamin B6 vitamers and pyridoxic acid in biological samples.

For the determination of vitamin B6 vitamers (pyridoxal phosphate, pyridoxamine phosphate, pyridoxal, pyridoxine, pyridoxamine) and 4-pyridoxic acid in biological samples such as plasma, cerebrospinal fluid and rat brain regions, a sensitive micromethod using high-performance liquid chromatography (HPLC) with fluorescence detection in combination with post-column derivatization is described. Metaphosphoric acid tissue extracts with deoxypyridoxine as an internal standard were injected into the HPLC system with a binary gradient elution at a flow-rate of 1.2 ml/min. The excitation wavelength of the fluorescence detector was set at 328 nm and the emission wavelength at 393 nm with a 15-nm slit width for the photocell. This method allows the assay of vitamin B6 vitamers within 30 min in one chromatographic run. The present method has been applied extensively for the measurement of vitamin B6 vitamer levels in discrete brain regions of small animals, cells in culture and biopsy samples.

Animals↗
PubMed1991

Domoic acid induced seizure activity in rats.

Domoic acid, in increasing doses (10-300 pmol), was microinjected into the hippocampal CA3 region of rats. All rats consistently exhibited generalized bilateral electrical seizure discharge activity at 100 pmol of domoic acid. Seizure latency varied inversely with the dose of domoic acid in the range tested. Local hippocampal administration of gamma-aminobutyric acid (GABA) resulted in neuronal recovery from domoic acid-induced seizures. The seizure activity of domoic acid might be the result of decreased GABAergic inhibition.

Action Potentials↗
PubMed1991

Transcriptional regulation of the glucokinase gene by biotin in starved rats.

The purpose of this work was to investigate whether biotin, a water-soluble vitamin, regulates the glucokinase gene. Biotin was administered intraperitoneally to starved rats, and the time course of glucokinase induction was followed over a time period of 12 h. The glucokinase mRNA was increased 19.6-fold during the first 1 h after biotin administration, afterwards rapidly decayed, and was hardly detectable by 4 h. The amount of glucokinase activity as determined by conventional enzyme activity assay increased in a time-dependent fashion, reaching 4-fold by 2 h of biotin administration. The transcriptional activity of the gene as measured by a nuclear run-on assay was increased about 6.7-fold within 45 min of biotin administration. These findings indicate that biotin can regulate the glucokinase gene at the transcriptional stage in the starved rat.

Albumins↗
PubMed1991

Increased calcium influx in caudal artery of rats made hypertensive with pyridoxine deficiency.

Moderate pyridoxine deficiency in rats has been shown to induce hypertension, which can be corrected by pyridoxine supplementation. In this study, calcium handling by isolated caudal arteries from pyridoxine-deficient and age-matched control rats was evaluated. We found 45Ca influx into the intracellular compartment to be significantly elevated in deficient rats. This increased influx could be attenuated with nifedipine, a calcium channel blocker, in a dose-dependent manner, suggesting alterations in the calcium channels that would make them leaky. The pyridoxine-deficient arterial segments maintained a higher resting tone; removal of extracellular calcium by EGTA or entry blockade by nifedipine decreased the tone significantly in the deficient arteries, compared with little or no effect in controls.

Animals↗
PubMed1990

Purification of dopa decarboxylase from bovine striatum.

Pyridoxal phosphate-dependent DOPA decarboxylase has been purified from bovine striatum to a specific activity of 1.6 U/mg protein. After ammonium sulfate precipitation (30-60%) it was purified by DEAE-Sephacel, Sephacryl S-200, and TSK Phenyl 5 PW chromatography. The purified enzyme showed a single silver straining band with polyacrylamide gel electrophoresis under both denaturing and non-denaturing conditions. The bovine striatal DOPA decarboxylase is a dimer (subunit Mr = 56,000 by SDS-PAGE) with a native Mr of 106,000 as judged by chromatography on Sephacryl S-200 and by sedimentation analysis. Similar to the DOPA decarboxylase purified from non-CNS tissues, the bovine striatal enzyme requires free sulfhydryl groups for activity, is strongly inhibited by heavy metal ions, and can decarboxylate 5-hydroxytryptophan as well. It should be noted, however, that the final enzyme preparation is enriched in DOPA decarboxylase activity. The distribution of the DOPA decarboxylase and 5-HTP decarboxylase activities also varies among several bovine brain regions. In addition, heat treatment of the enzyme preparation inactivated the two decarboxylation activities at different rates.

5-Hydroxytryptophan↗
PubMed1990

Alterations in brainstem alpha 2 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 alpha-methyl dihydroxyphenylalanine (alpha-methyl DOPA) also reduced the blood pressure of these animals to normal. There was also a significant increase in the Bmax 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 alpha 2 adrenoreceptors to endogenous norepinephrine.

Animals↗
PubMed1990

Influence of B vitamins on binding properties of serotonin receptors in the CNS of rats.

Treatment of normal adult rats with pyridoxine or a B-vitamin mixture resembling Neurobion led to an increase in serotonin content of various brain areas and to a decrease in the number of serotonin S2 receptors. The results indicate that the pyridoxal phosphate level in regions of the brain regulates the extent of decarboxylation of 5-hydroxytryptophan, the precursor of serotonin. The results also suggest a continuum from deficiency in pyridoxine to treatment of animals with a moderate excess of pyridoxine which is reflected in the synthesis and secretion into the synaptic cleft of the neurotransmitter serotonin.

Afferent Pathways↗
PubMed1989

Biotin.

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Animals↗
PubMed1989

Testicular function in biotin-deficient adult rats.

We have studied testicular function in the biotin-deficient rat biochemically and morphologically. Serum testosterone and luteinizing hormone (LH) levels were decreased significantly in the deficient rats. Administration of biotin or gonadotropins to the deficient rats reversed this decrease in serum testosterone. There was no difference in the serum cholesterol level between the control and biotin-deficient rats. A significant degree of sloughing of seminiferous tubule germinal epithelium was noticed in the biotin-deficient rat testes. Biotin treatment of biotin-deficient rats reversed this condition whereas testosterone treatment was without any effect. The development and maintenance of morphological and functional integrity of the seminiferous tubules appears to require a biotin-mediated step in addition to testosterone.

Animals↗
PubMed1988

Role of human serum biotinidase as biotin-binding protein.

Biotinidase shows two binding sites for biotin, with Kd = 59 and 3 nM respectively, and requires tryptophan and cysteine residues of the biotinidase protein for biotin-binding activity. Analysis of human serum by various column-chromatographic techniques indicates that biotinidase is the only protein which exchanges with labelled (+)-biotin. It was shown previously that epileptic patients receiving a high average dose of anticonvulsants (containing a carbamide group) have lower biotin concentrations than those receiving a low dose. We have shown in human serum and with purified biotinidase that these anticonvulsant drugs compete with biotin for binding to the protein moiety.

Amidohydrolases↗
PubMed1988

Pineal indoleamine metabolism in pyridoxine-deficient rats.

Pyridoxine deficiency causes physiologically significant decrease in brain serotonin (5-HT) due to decreased decarboxylation of 5-hydroxytryptophan (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 pyridoxine-deficient diet for 8 weeks. Pyridoxine deficiency did not alter the pattern of circadian rhythm of pineal 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), N-acetylserotonin (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 less than 0.05) in the pyridoxine-deficient animals. Treatment of pyridoxine-deficient rats with pyridoxine 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.

Animals↗