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Calcium metabolic changes and calbindin-D in experimental hypertension
C Hemmingsen1, M Staun, E Lewin
1Department of Nephrology, Rigshospitalet, University of Copenhagen, Denmark.
Insights
Hypertension alters calcium and magnesium metabolism, affecting calbindin-D levels differently across models. This suggests cellular resistance to vitamin D in some hypertensive rats.
Area of Science:
- Nephrology
- Endocrinology
- Calcium Metabolism
Background:
- Calbindin-D proteins are crucial for calcium absorption and transport.
- Hypertension is associated with complex alterations in mineral metabolism.
- Understanding these relationships is key to managing hypertensive conditions.
Purpose of the Study:
- To investigate renal and intestinal calbindin-D levels in relation to calcium and magnesium metabolism.
- To analyze these changes across three distinct experimental hypertension models.
Main Methods:
- Utilized spontaneously hypertensive rats (SHR), Dahl salt-sensitive (Dahl-S) rats, and Goldblatt renovascular hypertension models.
- Measured calbindin-D28k (renal) and calbindin-D9k (intestinal) concentrations.
- Assessed plasma levels of calcium, magnesium, 1,25(OH)2 vitamin D, and parathyroid hormone.
Main Results:
- SHR showed decreased renal and intestinal calbindin-D, hypocalcemia, hypomagnesemia, and elevated 1,25(OH)2 vitamin D.
- Dahl-S rats exhibited reduced intestinal calbindin-D9k and increased 1,25(OH)2 vitamin D.
- Renovascular hypertension led to increased intestinal calbindin-D9k, 1,25(OH)2 vitamin D, PTH, and magnesium, with unaffected renal calbindin-D28k and plasma calcium.
Conclusions:
- Three hypertension models display distinct calbindin-D regulation patterns linked to calcium/magnesium metabolism.
- All models showed increased plasma 1,25(OH)2 vitamin D during hypertension.
- SHR and Dahl-S rats suggest cellular resistance to 1,25(OH)2 vitamin D impacting calbindin-D expression.
Objective:
To examine renal and intestinal calbindin-D in relation to calcium metabolic changes in three different models of experimental hypertension.
Design:
Spontaneously hypertensive rats (SHR), hypertension-prone Dahl salt-sensitive (Dahl-S) rats and the Goldblatt two-kidney, one clip rat model of renovascular hypertension were examined.
Results:
Both prehypertensive and hypertensive SHR had significantly lower concentrations of both renal calbindin-D28k and intestinal calbindin-D9k than Wistar control rats. This was accompanied by hypocalcaemia, hypomagnesaemia and increased plasma 1,25(OH)2 vitamin D levels. Induction of hypertension in Dahl-S rats reduced intestinal calbindin-D9k and increased plasma levels of 1,25(OH)2 vitamin D, while renal calbindin-D28k levels, plasma calcium levels and plasma magnesium levels were unchanged. Renovascular hypertension was associated with a significant increase in the intestinal calbindin-D9k, plasma 1,25(OH)2 vitamin D, parathyroid hormone and magnesium levels, while renal calbindin-D2k, plasma calcium and phosphorus levels were unaffected.
Conclusions:
These three models of experimental hypertension have clearly demonstrated three separate patterns in the regulation of renal and intestinal calbindin-D, which relate to different alterations of factors involved in calcium and magnesium metabolism. In all three models hypertension was accompanied by a significant increase in plasma concentrations of 1,25(OH)2 vitamin D. Only rats with renovascular hypertension showed increased intestinal calbindin-D9k levels, whereas reduced concentrations were found in the SHR and in the hypertensive Dahl-S rats. This indicates the existence of a resistance at the cellular level to 1,25(OH)2 vitamin D affecting the expression of calbindin-D in both SHR and Dahl-S rats.