Dietary magnesium deficiency enhances vasoconstriction and susceptibility to nifedipine in rat aortas through H7-sensitive modulation of L-type Ca2+ channels via alpha 1-adrenoceptor stimulation.
Magnesium deficiency may modulate vascular calcium channel sensitivity in rat models; leaves open any clinical relevance to human hypertension or calcium blocker therapy.
The mechanisms underlying the enhanced contractile response to phenylephrine (PE) and increased susceptibility to nifedipine of de-endothelialized thoracic aorta isolated from rats with dietary magnesium deficiency (Mg-deficient rats) were examined by functional and radioligand binding studies. Enhanced PE-induced contractions and increased susceptibility to nifedipine in Mg-deficient rats were not observed in the presence of 10 microM H7. PE significantly decreased the KD value without changing Bmax in the binding of [3H]PN200-110 to de-endothelialized aortic strips. The KD value obtained in the Mg-deficient rats was significantly smaller than that in the controls. Nifedipine displaced the binding of [3H]PN200-110 concentration-dependently, and the pKi value in Mg-deficient rats was significantly larger than that in the controls. A combination of PE and H7 abolished this difference. These results indicate that the modulation of L-type Ca2+ channels via the stimulation of alpha 1-adrenoceptors may be involved in the enhancement of vasoconstriction and increased susceptibility to nifedipine in aortas isolated from Mg-deficient rats. The H7-sensitive mechanisms may play an important role in these phenomena.
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Sakaguchi et al. (1994) studied this question.
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