Abnormal magnesium metabolism in two rat models of genetic hypertension

Abstract

Magnesium concentrations in erythrocyte ghosts and arterial tissue of male, spontaneously hypertensive rats (SHR) were significantly less than in these tissues of male normotensive controls (Wistar-Kyoto; WKY) of the same age, which were also fed rat chow and tap water. The magnesium concentration in SHR erythrocyte ghosts was increased to the control value by incubating SHR erythrocytes with WKY blood plasma; SHR plasma did not affect the magnesium concentration in WKY erythrocyte ghosts. The magnesium concentrations in erythrocyte ghosts, aortas, and mesenteric arteries from female salt-sensitive (SS/JR) and salt-resistant (SR/JR) Dahl-derived rats, both maintained ad libitum on laboratory rat chow and either tap water or 0.9% NaCl, were not different but were significantly less than those of Sprague-Dawley rats considered as controls. While the ingestion of 0.9% NaCl had no effect on the magnesium concentrations measured in these animals, it caused the salt-sensitive rats to become severely hypertensive. It is evident from these observations that the decreased binding of magnesium to the plasma membrane of cells may be an inheritable metabolic defect that may be associated with the development of hypertension. However, in those instances of hypertension in which this defect occurs, it appears to be a contributing cause of the hypertension; by itself the defect is not a cause of hypertension.

Peptidomic Identification and Biological Validation of Neuroendocrine Regulatory Peptide-1 and -2

“…These in vivo and immunocytochemical observations suggest that NERPs are involved in the central control of body fluid balance. Consistent with previous reports (25,26), icv injection of hypertonic NaCl or AII increased plasma vasopressin levels in rats (Fig. 4C, 2nd and 11th lanes).…”

“…Vasopressin release is regulated by the electrical activity of vasopressin neurons, which are modulated by various neurotransmitters and neuromodulators (25,26). The major neural signals to vasopressin neurons are excitatory and inhibitory postsynaptic currents generated by presynaptic release of glutamate and ␥-aminobutyric acid, respectively.…”

Abnormal Ca2+ Handling and Increased Mg2+ Permeability in Platelets of Hypertensive Rats.

“…However, in contrast to the results predicted by this hypothesis, the present study reveals that platelet [Mg2+]i was increased and serum Mg2+ was unaltered in SHR in the present study. Many investigators have shown decreased [Mg2+]i in erythrocytes and platelets in essential hypertension (16-18) and in erythrocytes and cardiac tissue in SHR (19)(20)(21). The reason for these discrepancies between our present findings and those of previous reports is not clear but may be due to the differences in cell types studied and the methods used for [Mg2+]i assessment.…”

“…For example, it has been suggested that there is an important connection between elevated [Ca2+]i and increased Na+/ H+ exchange activity (12) or intracellular Na+ accumulation via suppression of Na+/K+ATPase (13, 14). Furthermore, a number of reports have shown Mg2+ deficiency at the cellular or systemic levels in essential hypertensive patients (9, 15-18) and genetically hypertensive rats (19)(20)(21), although a few studies have not (22,23). In theory, Mg2+ deficiency in the cytosol may account for decreases in Ca2+-ATPase and Na+/K+ATPase and increases in Na+-Ca2+ exchange, thereby leading to increased intracellular Ca2+ concentrations (24,25).…”

Low [Mg 2+ ] e Enhances Arterial Spontaneous Tone via Phosphatidylinositol 3-Kinase in DOCA-Salt Hypertension

“…11,14,28,29 In humans, the occurrence of Mg 2ϩ deficiency and the benefits of Mg 2ϩ supplementation have been debated, largely by which end point and how to measure Mg 2ϩ . 30 -33 However, even small alterations in Mg 2ϩ might induce vascular alterations, increasing the risk for cardiovascular-related conditions.…”