Importance of decreased intracellular phosphate and magnesium concentrations and reduced ATPase activities in spontaneously hypertensive rats

Citation
K. Kisters et al., Importance of decreased intracellular phosphate and magnesium concentrations and reduced ATPase activities in spontaneously hypertensive rats, MAGNES RES, 13(3), 2000, pp. 183-188
Citations number
41
Categorie Soggetti
Biochemistry & Biophysics
Journal title
MAGNESIUM RESEARCH
ISSN journal
09531424 → ACNP
Volume
13
Issue
3
Year of publication
2000
Pages
183 - 188
Database
ISI
SICI code
0953-1424(200009)13:3<183:IODIPA>2.0.ZU;2-P
Abstract
A decrease in total magnesium content is not a direct proof of a decreased magnesium ion concentration. It could reflect a phosphate alteration or an ATP metabolism disorder. Plasma phosphate levels are lower in spontaneously hypertensive rats (SHRs) than in Wistar-Kyoto (WKY) rats, and defects in m embrane regulation or mitochondrial ATP synthase occur. Only sparse data ex ist concerning cellular magnesium and phosphate concentrations in hypertens ive cells. In aortic smooth muscle cells from 10 SHRs of the Munster strain and 10 age-matched normotensive WKY rats, the intracellular phosphate and magnesium content was measured by electron probe X-ray microanalysis (Camsc an CS 24 apparatus, Cambridge, U.K.). The Mg++ content was 0.90 +/- 0.15 g/ kg dry weight in SHRs versus 1.15 +/- 0.10 g/kg dry weight in WKY rats (p<0 .05). Vascular smooth muscle phosphate content was 23.6 +/- 0.79 g/kg dry w eight in WKY rats versus 15.81 +/- 1.22 g/kg dry weight in SHRs (p<0.01). I n seven animals, erythrocytic ATP content was 180.2 +/- 102 in SHRs vs. 432 +/- 72 mu mol/L cells in WKY rats (p<0.01). The Na+/K+-ATPase activity was significantly decreased in hypertensive animals as compared to controls (6 .49 +/- 2.3 vs. 12.64 +/- 2.9 nmol inorganic phosphate/mg protein/min (p<0. 01)). Aortic smooth muscle cells from SHRs are characterized by markedly lo wered cellular phosphate and magnesium concentrations and an altered ATP me tabolism, possibly due to a membrane defect or a magnesium deficit in hyper tensive cells.