Reduction in dietary vitamin E prevents onset of hypertension in developing spontaneously hypertensive rats

1979 ◽  
Vol 35 (12) ◽  
pp. 1561-1562 ◽  
Author(s):  
C. R. Pace-Asciak ◽  
M. C. Carrara
1995 ◽  
Vol 15 (3) ◽  
pp. 401-414 ◽  
Author(s):  
Satoru Moriguchi ◽  
Keisei Maekawa ◽  
Mariko Okamura ◽  
Keiko Oonishi ◽  
Yasuo Kishino

1987 ◽  
Vol 253 (4) ◽  
pp. F712-F718
Author(s):  
C. H. Hsu ◽  
C. S. Yang ◽  
S. R. Patel ◽  
M. G. Stevens

We have studied the effect of dietary vitamin D restriction on serum levels of vitamin D metabolites in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Both WKY and SHR were fed a vitamin D-deficient or a vitamin D-supplemented diet beginning at 4 wk of age. In vitamin D-supplemented animals, the serum 1,25-dihydroxycholecalciferol [1,25(OH)2D3] concentration of WKY (55.4+/- 6.6 pg/ml, n = 5) was similar to the level of SHR (46.3+/- 5.9 pg/ml, n = 5). Plasma calcium concentration was not different between WKY and SHR. In animals fed a vitamin D-deficient diet, the serum concentration of 1,25-(OH)2D3 of SHR (23.0+/- 1.3 pg/ml, n = 5) was significantly lower than that of WKY (67.6+/- 4.6 pg/ml, n = 5, P less than 0.01). Plasma 25-hydroxycholecalciferol level was markedly decreased in both WKY (3.6+/- 0.5 ng/ml, n = 7) and SHR (2.8+/- 0.4 ng/ml). The SHR, but not the WKY, developed hypocalcemia (WKY, 9.68 mg/dl; SHR, 6.70 mg/dl). Despite hypocalcemia, fasting urinary Ca2+ excretion of SHR exceeded that of WKY. We conclude that the lower 1,25(OH)2D3 level in SHR fed a vitamin D-deficient diet may be due to a defect in the synthesis of 1,25(OH)2D3. The low level of 1,25(OH)2D3 is associated with renal wasting of calcium and hypocalcemia in SHR.


1979 ◽  
Author(s):  
A. Kuramoto ◽  
H. Okita ◽  
S. Koganemaru

The increase of platelet production was demonstrated in stroke-prone SHR(SHRSP) after 10 weeks of age, probably due to increased platelet consumption compared with those in stroke-resistant SHR(SHRSR)(Koganemaru, S., et al. Thrombus. Haemostas.(Stuttgart)38:139, 1977). We extended our study to see the effect of aging, blood pressure, platelet-inhibiting drug and vitamin E(Vit.E) on this kinetic change. SHRSP(A1-sbF37-39) and SHRSR (BlF36-38) with matched age (5 weeks, 10 weeks and 9-12 months) and sex were used. The maximum uptake of 75se-methionine(75SeM) into platelets was not affected in both salt loading group and Clonidine group in SHRSP. A significant decrease was observed in dipyridamole group (0.096 ± 0.020, p<0.05). The platelet survival time was shortened in Vit. E deficient group of SHRSR; 3.0 days at 9-10 weeks. In Vit.E sufficient group of SHRSP. the platelet survival time was corrected to normal. The maximum uptake of 75SeM increased in both Vit.E deficient group of SHRSP (0.119 ± 0.010 vs 0.192 ± 0.030, p<0.01) and SHRSR (0.071 ± 0.016 vs 0.119 ± 0.018, p<0.01). The increased platelet production was not affected by blood pressure but it can be suppressed by treating with dipyridamole or giving Vit.E before 10 weeks of age.


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