Kisters L1, Micke O2, Noack T2,3, Gröber U2,4, Kisters K1,2,4

1Med. Klinik, St. Anna Hospital & ESH Excellence Centre, Herne, Ruhr University Bochum,DE

2 Gesellschaft für Magnesiumforschung, Tutzing, DE

3Institute für Physiologie, University Rostock, DE

4 AMM – Academy of micronutrient medicine, Essen, DE

 

Alterations in the metabolism of calcium and magnesium are involved in the pathogenesis of essential hypertension. (1-7) Serum magnesium concentrations only insufficiently reflect disorders in magnesium handling in humans, as only about 1% of total body magnesium stores are in blood.The calcium and magnesium flux across the external membrane is regulated by a calcium pump (calcium-magnesium-ATPase), calcium and magnesium (TRPM 6 and 7) channels and a sodium magnesium antiport. An increased calcium- magnesium ratio is known to be involved in the development of atherosclerosis. Early onset of this disorders are known in hypertension. (3)  In animals this phenomenon has also been described. (4)

We now present a study in18  hypertensive elderly concerning ionized magnesium concentrations and ionized calcium/magnesium ratio in blood measured by a Prime Plus apparatus by Nova Medical, Rödermark, Germany.

In 18 elderly hypertensives (9 male/9 female with normal renal function) ionized magnesium was measured 0.55+/-0.04 mmol/L (normal range: 0.54 – 0.80 mmol/L).

The ionized calcium/ionized magnesium ratio was 2.33+/-0.18 (normal range below 2.40).

About 40% of elderly hypertensives had an increased ratio of ionized calcium and magnesium, which is known to be a marker for the development of artheriosclerosis.

In conclusion as described earlier, a magnesium deficiency can be involved in the pathogenesis of hypertension in elderly showing a link to arteriosclerosis development.

 

References

  1. Phair RD. (1988.) Cellular calcium and atherosclerosis: a brief review. Cell Calcium. 9(5-6): 275-284.
  2. Kisters K, Tepel M, Spieker C, Dietl KH, Barenbrock M, Rahn KH, Zidek W. (1997). Decreased caellular Mg++ concentrations in a subgroup of hypertensives – cell models for the pathogenesis of primary hypertension. J Hum Hypertens. 11: 367-372.
  3. Kosch M, Hausberg M, Westermann G, Köneke J, Matzkies F, Rahn KH, Kisters K. (2001). Alterations in calcium and magnesium content of red cell membranes in patients with primary hypertension. Am J Hypertens. 14: 254-258.
  4. Kisters K, Wessels F, Tokmak F, Krefting ER, Gremmler B, Hausberg M. (2004). Early-onset increased calcium and decreased magnesium concentrations and an increased calcium/magnesium ratio in SHR versus WKY. Magnes Res.17(4): 264-269.
  5. Kisters K, Wessels F, Küper H, Tokmak F, Krefting ER, Gremmler B, Kosch M, Barenbrock M, Hausberg M. (2004). Increased calcium and decreased magnesium concentrations and an increased calcium/magnesium ratio in spontaneously hypertensive rats versus Wistar-Kyoto rats: Relation to arteriosclerosis. Am J Hypertens. 17: 59-62.
  6. Gröber U, Schmidt J, Kisters K. (2015). Magnesium in prevention and therapy. Nutrients. 23: 8199-8226.
  7. Kisters K, Gröber U, Gremmler B, Sprenger J, Wroblewski F, Deutsch A, Kisters L, Westhoff T, Kolisek M. (2020). Ionized magnesium deficiency in elderly hypertensive patients – a pilot study. Nutr Food Sci J. 3(2): 129-134.