Intracellular Mg++ concentrations in smooth and striated muscle cells in spontaneously hypertensive rats

Abstract

Decreased intracellular Mg++ concentrations seem to be involved in the pathogenesis of primary hypertension. Of special interest is the smooth muscle cell with its electrolyte metabolism in primary hypertension, but also heart muscle cells and their Mg++ concentrations are of growing interest. Therefore, in aortic smooth muscle cells and striated heart muscle cells (left ventricle) from 20 spontaneously hypertensive rats (SHR) of the Münster strain and 20 normotensive Wistar-Kyoto rats (WKY), the intracellular Mg++ content was measured. The electron probe x-ray microanalysis technique was used to determine intracellular Mg++ concentrations under nearly in vivo conditions in aortic cryosections 3 microm thick and striated heart muscle cells 4 microm thick (Camscan CS 24 apparatus). Vascular smooth muscle Mg++ content was 36.4 +/- 3.1 mmol/kg dry weight in SHR versus 48.6 +/- 3.7 mmol/kg dry weight in WKY (P < .001). In striated heart muscle cell Mg++ concentrations, there was no significant difference in SHR and WKY (79.9 +/- 5.6 versus 80.3 +/- 5.9 mmol/ kg dry weight). In conclusion, the present study revealed that genetic hypertension in the spontaneously hypertensive rat is accompanied by significantly decreased intracellular Mg++ concentrations in vascular smooth muscle cells. In striated heart muscle cells, Mg++ content was not significantly different in SHR and WKY. Mg++ handling is different in vascular smooth muscle and striated heart muscle cells in WKY and SHR (P < .01).

Metabolic characteristics of soleus muscle in relation to insulin action in the offspring of hypertensive parents

“…A study by Hajek et al [14] showed an increase in PCr/Pi, PCr/bATP, PCr/Patp, and PDE/bATP ratios and a decrease in Pi/PDE, PCr/PME, and Pi/Patp ratios in the skeletal muscle of hypertensive individuals, and Sebekova et al [31] showed a lower ATP/Pi ratio and a higher PCr/ATP ratio in the skeletal muscle of insulinresistant patients with impaired kidney function. Lower phosphate content was found in the aortic smooth muscle cells in SHR [30].…”

“…The study by Jelicks et al [32] confirmed Mgi depletion in heart muscle cells, whereas the study by Kisters et al [30] did not demonstrate any difference. Conditions with reduced aortal distensibility, which represent a prerequisite for the development of hypertension, are also associated with a decrease in Mgi in skeletal muscle cells [33].…”

“…Contrasting data were obtained in the study by Sasaki [27], who did not report any reduction in Mgi in the lymphocytes of spontaneously hypertensive rats (SHR). More relevant to the study of hypertension are the findings of magnesium depletion in vascular smooth muscle cells in the aorta and skeletal muscle of SHR [28][29][30]. By contrast, Sebekova et al [31] did not find any differences in Mgi levels in skeletal muscle cells in insulin-resistant patients with impaired kidney function, and Hajek et al [14] did not demonstrate any significant difference in Mgi levels in skeletal muscle in hypertensive patients.…”

Positive Effect of Magnesium Orotate Therapy in Hypertensive Heart Disease

“…Many basic studies have shown that magnesium deficiency might be involved in the development of essential hypertension or borderline hypertension [14][15][16][17][18][19][20][21][22][23][24][25][37][38][39][40][41].…”

Intracellular Mg 2+ hyperpolarizes rabbit coronary artery smooth muscle cells by differential modulation of Ca 2+ i -dependent ion channels

“…For patients with exercise-and hyperventilation-induced angina or preeclampsia, intravenous infusion of Mg 2+ is effective [11,20,33]. A role for intracellular Mg 2+ in the pathogenesis of essential hypertension has been suggested in a recent study showing that [Mg 2+ ] i in vascular smooth muscle is significantly lower in spontaneously hypertensive rats, whereas that in skeletal myocytes does not differ between hypertensive and normal rats [10]. The mechanisms of the effect of Mg 2+ on vascular tone have been investigated widely [35,36], but little is known about the mechanism by which intracellular Mg 2+ regulates vascular tone.…”