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1. High calcium diet attenuates the development of hypertension but an associated undesirable effect is that Mg2+ loss to the urine is enhanced. Therefore, we studied the effects of high calcium diet alone and in combination with increased magnesium intake on blood pressure and arterial function. 2. Forty-eight young spontaneously hypertensive rats (SHR) were allocated into four groups, the dietary contents of Ca2+ and Mg2+ being: 1.1%, 0.2% (SHR); 2.5%, 0.2% (Ca-SHR); 2.5%, 0.8% (CaMg-SHR); and 1.1%, 0.8% (Mg-SHR), respectively. Development of hypertension was followed for 13 weeks, whereafter electrolyte balance, lymphocyte intracellular free calcium ([Ca2+]i), and mesenteric arterial responses in vitro were examined. Forty normotensive Wistar-Kyoto (WKY) rats were investigated in a similar manner. 3. Calcium supplementation comparably attenuated the development of Lypertension during normal and high magnesium intake in SHR, with an associated reduced lymphocyte [Ca2+]i and increased Mg2+ loss to the urine. 4. Endothelium-dependent arterial relaxation to acetylcholine was augmented in Ca-SHR and CaMg-SHR, while the relaxations to isoprenaline and the nitric oxide donor SIN-1 were similar in all SHR groups. Relaxation responses induced by the return of K+ to the organ bath upon precontractions in K(+)-free solution were used to evaluate the function of arterial Na+, K(+)-ATPase. The rate of potassium relaxation was similar in Ca-SHR and CaMg-SHR and faster than in untreated SHR. 5. Contractile responses to high concentrations of potassium and noradrenaline, and the ability of vascular smooth muscle to sequester Ca2+, which was evaluated by eliciting responses to caffeine or noradrenaline after loading periods in different Ca2+ concentrations, were comparable in all SHR groups. In SHR with increased magnesium intake, and in WKY rats with calcium or magnesium supplementation, no detectable effects on blood pressure and arterial function were observed.6. In conclusion, high calcium diet attenuated the development of hypertension in SHR, with an associated augmented endothelium-dependent relaxation, promoted recovery rate of ionic gradients across the cell membrane via Na+, K+-ATPase, and reduced basal [Ca2+ ]i. Dietary magnesium supplementation, whether combined with normal or high calcium intake, had no beneficial effects on blood pressure or arterial function.
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M Kähönen, and
P Arvola, and
H Wuorela, and
H Vapaatalo, and
I Pörsti
June 1989,
Hypertension (Dallas, Tex. : 1979),
H Mäkynen, and
M Kähönen, and
P Arvola, and
H Wuorela, and
H Vapaatalo, and
I Pörsti
January 1992,
Archives internationales de physiologie, de biochimie et de biophysique,
H Mäkynen, and
M Kähönen, and
P Arvola, and
H Wuorela, and
H Vapaatalo, and
I Pörsti
November 2003,
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H Mäkynen, and
M Kähönen, and
P Arvola, and
H Wuorela, and
H Vapaatalo, and
I Pörsti
December 1995,
Clinical and experimental pharmacology & physiology. Supplement,
H Mäkynen, and
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I Pörsti
May 1994,
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H Mäkynen, and
M Kähönen, and
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H Vapaatalo, and
I Pörsti
January 1989,
Magnesium,
H Mäkynen, and
M Kähönen, and
P Arvola, and
H Wuorela, and
H Vapaatalo, and
I Pörsti
January 1989,
Clinical and experimental hypertension. Part A, Theory and practice,
H Mäkynen, and
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I Pörsti
January 1986,
Magnesium,
H Mäkynen, and
M Kähönen, and
P Arvola, and
H Wuorela, and
H Vapaatalo, and
I Pörsti
March 1989,
American journal of hypertension,
H Mäkynen, and
M Kähönen, and
P Arvola, and
H Wuorela, and
H Vapaatalo, and
I Pörsti
June 1997,
Biochemical pharmacology,
