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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.