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Regulation of calcium influx into vascular smooth muscle by vitamin B6
K J Lal1, S K Sharma, K Dakshinamurti
1Department of Biochemistry and Molecular Biology, University of Manitoba, Faculty of Medicine, Winnipeg, Canada.
Insights
Vitamin B6 deficiency causes hypertension by increasing calcium influx into vascular smooth muscle. Vitamin B6 compounds block this calcium influx, suggesting a role for dihydropyridine-sensitive calcium channels in hypertension.
Area of Science:
- Cardiovascular Physiology
- Nutritional Biochemistry
Background:
- Vitamin B6 deficiency-induced hypertensive (B6DHT) rats exhibit elevated calcium influx into vascular smooth muscle.
- Understanding the mechanisms of hypertension in B6DHT rats is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of calcium channels in the hypertension of B6DHT rats.
- To determine if vitamin B6 vitamers can modulate calcium influx in B6DHT rats.
Main Methods:
- Assessing in vitro calcium influx in caudal artery segments from B6DHT and control rats.
- Utilizing pharmacological agents like BAY K 8644, Nifedipine, and pyridoxal phosphate to probe calcium channel activity.
Main Results:
- Vitamin B6 vitamers inhibited calcium influx in B6DHT rat arteries.
- BAY K 8644 did not further increase calcium influx in B6DHT rat arteries.
- BAY K 8644 antagonized the effects of Nifedipine and pyridoxal phosphate, indicating dihydropyridine-sensitive calcium channel involvement.
Conclusions:
- The dihydropyridine-sensitive calcium channel is a key site of the calcium influx defect in B6DHT rat hypertension.
- Vitamin B6 supplementation may offer a therapeutic strategy for managing hypertension by targeting calcium channels.
Abstract:
In the vitamin B6 deficiency-induced hypertensive (B6DHT) rat there is an increased influx of calcium into the vascular smooth muscle. Vitamers which possess vitamin B6 activity blocked the in vitro calcium influx into the caudal artery of B6DHT rats and the BAY K 8644-induced influx into artery segments from vitamin B6-supplemented (control) rats. BAY K 8644 did not increase further the calcium influx into caudal artery segments from B6DHT rats. However, when this influx was partly decreased by Nifedipine or by pyridoxal phosphate, BAY K 8644 antagonized their effects indicating that calcium influx mediated by the dihydropyridine-sensitive calcium channel is a site of the calcium influx defect in the B6DHT rat.