I. Weanling Wistar rats were pair fed for 10 weeks on a purified diet containing either normal or suboptimal quantities of magnesium (960 or 80 mg/kg respectively).2. At week 2, hypomagnesaemia was accompanied by hypertriglyceridaemia, an increase in plasma cholesterol and a decrease in high-density-lipoprotein-cholesterol in animals fed on the Mg-deficient diet. At week 10, the increase in triglycerides observed in Mg-deficient animals was less marked while the increase in total cholesterol was more important.3. During the whole experimental period, Mg-deficient animals never showed hypertension. At week 2, mean arterial blood pressure was significantly lower in Mg-deficient rats than in their respective controls, while heart rate was significantly increased. However, hypotension accompanied by tachycardia was a transitory phenomenon which appeared only in the early phase of deficiency.4. Vascular reactivity was studied in vagotomized anaesthetized rats after ganglionic blockade with pentolinium and atropine sulphate. The reactivity to noradrenaline was significantly higher in Mg-deficient rats compared with pair-fed controls after 2 weeks on the experimental diet.
Magnesium balance, and plasma and urinary levels, were studied in spontaneously hypertensive (SHR), Wistar Kyoto (WKY) and in Wistar (WI) rats. We found few differences in the measured parameters between WKY and WI rats, but the SHR rat which similarly maintained Mg balance has lower plasma Mg levels and less urinary Mg excretion. These abnormalities could favor establishment or maintenance of hypertension.
Total plasma concentrations of bromine, copper, rubidium, selenium and zinc were measured in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) of 5-20 weeks of age, using an X-ray fluorescence spectrometry technique. Although plasma levels of bromine, rubidium, selenium and zinc varied at different ages when comparing SHR and WKY, their general evolution was similar. Copper levels increased more in SHR than in WKY. These perturbations in trace element levels could perhaps participate in the establishment of hypertension in SHR, but could also be due to genetic differences between the strains, unrelated to the development of hypertension.
In order to define relationships between hypertension and calcium metabolism, we have studied calcium metabolism in Lyon genetically hypertensive rats (LH) and their two normotensive controls (LN and LL). The total and ionized plasma calcium levels were slightly but significantly decreased in the LH compared to LN and LL from 4 to 23 weeks of age. During this period, dietary calcium intake was decreased in LH rats but urinary and fecal excretions did not differ. Intestinal utilization and balance were impaired during development of hypertension in LH rats. Thus minor alterations in calcium metabolism differentiate the LH rat from its normotensive controls.
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