These are some interesting articles that show calcium-channel-blocking effects of pyridoxine (vitamin B6) or its metabolites (pyridoxamine, pyridoxal, pyridoxal-5'-phosphate, etc.) [Dakshinamurti et al., 1998: (http://www.ncbi.nlm.nih.gov/pubmed/9823019); Lal and Dakshinamurti, 1993: (http://www.ncbi.nlm.nih.gov/pubmed/7510735)]. The idea that these researchers have is that the calcium-channel-blocking effects are responsible for the antihypertensive effects that pyridoxine has sometimes been found to produce. Viswanathan et al. (1991) [Viswanathan et al., 1991: (http://www.ncbi.nlm.nih.gov/pubmed/1645979)] found that the influx of calcium into the arteries of pyridoxine-deficient rats was elevated in comparison to the calcium influx in control rats. I find it hard to believe that pyridoxine is exerting a pharmacological, non-cofactor-related effect on calcium channels, but maybe it's some strange result of a metabolic effect of pyridoxine.
Some of the effects of pyridoxine on calcium influx could be related to the changes in the serum alkaline phosphatase (ALP) concentrations in response to changes in pyridoxine status.
Lal and Dakshinamurti (1995) [Lal and Dakshinamurti, 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7622854)] found that either very low dietary calcium or pyridoxine increased the systolic blood pressure in rats, and the combination of dietary pyridoxine and calcium depletion produced additive or synergistic increases in blood pressure. It's reasonable to think that there's some increase in calcium influx into smooth muscle cells in response to pyridoxine depletion, but it's not clear what the mechanism underlying that increase would be. Based on the articles about pyridoxine or vitamin D, either of which can change the serum ALP levels, I can't get a good handle on the mechanisms leading to an increase or decrease in ALP levels. Matyaszczyk et al., (1993) [Matyaszczyk et al., 1993: (http://www.ncbi.nlm.nih.gov/pubmed/8429369) (http://jn.nutrition.org/cgi/reprint/123/2/204.pdf)] found that pyridoxine deficiency tripled the serum ALP level and nonsignificantly elevated serum calcium. Those researchers also found that pyridoxine repletion elevated the intracellular calcium levels in enterocytes, but those effects on enterocytes would be expected to be unique to that cell type and wouldn't shed light on the effects of pyridoxine on calcium influx into smooth muscle cells. A change in the serum ALP concentration, producing an increase in extracellular ALP activity, can apparently increase the intracellular PLP levels and decrease (or fail to change) the extracellular PLP levels [Baumgartner-Sigl et al., 2007: (http://www.ncbi.nlm.nih.gov/pubmed/17395561)]. ALP cleaves PLP into pyridoxal, and pyridoxal can then enter cells and be converted into PLP intracellularly (Baumgartner-Sigl et al., 2007). There's some underlying set of mechanisms by which pyridoxine may be able to alter calcium influx into some cell types and also change the activity of ALP. The apparent decrease in ALP in response to pyridoxine supplementation may be some compensatory change that would tend to prevent excessive intracellular PLP concentrations, given that a decrease in PLP activity, such as could be produced by something like a change in the intake of vitamin D, independently of any change in pyridoxine intake, would be expected, given the results of these articles, to reduce the cleavage of extracellular PLP into pyridoxal and thereby reduce intracellular pyridoxal and intracellular PLP levels. But I don't know what the underlying mechanism would be. But that's one area in which a change in calcium or vitamin D intake could conceivably influence pyridoxine metabolism.
It's interesting that serum ALP levels are increased as a result of cirrhosis or cholestatic liver disease [Fontana et al., 1998: (http://hera.ugr.es/doi/15001921.pdf) (http://www.ncbi.nlm.nih.gov/pubmed/9566836)], and this could conceivabl I wonder if an increase in ALP levels from something like liver disease, independently of any change in pyridoxine intake, would necessarily increase intracellular PLP levels. Presumably it wouldn't, because the pyridoxal, produced by the ALP-mediated cleavage of extracellular PLP, could either enter cells again or be degraded into pyridoxic acid. The conversion of pyridoxal into pyridoxic acid is catalyzed by either aldehyde dehydrogenase or aldehyde oxidase enzymes. Pyridoxic acid is a "dead-end" metabolite of pyridoxine that's excreted. So the pyridoxal could be cleaved by ALP in some tissue or extrahepatic site and then either transported into extrahepatic cells or metabolized into pyridoxic acid in the liver, etc.
It's worth noting, in light of that article using extremely low dietary calcium to induce hypertension [Lal and Dakshinamurti, 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7622854)], that a moderate calcium intake is, particularly in the context of a reasonable vitamin D intake, unlikely to cause thrombogenicity, but there's been a trend toward very high calcium intakes and inadequate magnesium intake (http://hardcorephysiologyfun.blogspot.com/2009/01/calcium-magnesium-serum-calcium-vitamin.html). There is some evidence that an adequate calcium intake can help control blood pressure in humans, too, but an excess of dietary calcium could potentially reduce magnesium absorption and produce thrombogenicity or hypertension by that mechanism. I've seen clinical trials using 3,000 mg of supplemental calcium, along with the dietary intake. That seems really excessive to me, and calcium is being added to orange juice and everything else. A reasonable intake of 500-1,000 mg/d, from both food and any supplemental calcium, seems more reasonable, especially in combination with something like vitamin D. It's interesting that vitamin D also increases magnesium absorption and not just calcium absorption. Vitamin D may also increase urinary magnesium loss, but it's not clear that this increase abolishes the "benefits" of an increase in magnesium absorption. A lot of the effects of magnesium are extracellular, actually, and there's a lot that's not known about magnesium metabolism. Those articles in my past posting are really in-depth, though, and there definitely seems to be some potential for hypercoagulability and thrombogenicity from very high dietary calcium intakes and low dietary or supplemental magnesium intakes. The same thing could conceivably occur with vitamin D, but vitamin D has all these effects of reducing calcium influx (upregulating L-type calcium channels, etc.). I think those effects, along with the increases in magnesium absorption, might tend to offset the potential procoagulant effect, produced by an increase in the vitamin D intake, of a slight increase in serum calcium by vitamin D.
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