Decreased intracellular phosphate and magnesium concentrations in vascular smooth muscle cells from spontaneously hypertensive rats

Abstract

A decrease in total magnesium content is not a direct proof of a decreased magnesium ion concentration. It could reflect a phosphate alteration or an ATP metabolism disorder. Plasma phosphate levels are lower in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto rats (WKY), and defects in membrane regulation or mitochondrial ATP synthase occur. Only sparse data exist concerning cellular magnesium and phosphate concentrations in hypertensive cells. In aortic smooth muscle cells from 10 SHR of the Münster strain and 10 age-matched normotensive WKY, the intracellular phosphate and magnesium content was measured by electron probe X-ray microanalysis (Camscan CS 24 apparatus, Cambridge, U.K.). The Mg(++) content was 0.90 +/- 0.15 g/kg dry weight in SHR versus 1.15 +/- 0.10 g/kg dry weight in WKY (p < 0.05). Vascular smooth muscle phosphate content was 23.6 +/- 0.79 g/kg dry weight in WKY versus 15.81 +/- 1.22 g/kg dry weight in SHR (p < 0.01). Aortic smooth muscle cells from SHR are characterized by markedly lowered cellular phosphate and magnesium concentrations and an altered ATP metabolism. </hea

Decreased Erythrocyte NA+,K+-ATPase Activity and Increased Plasma TBARS in Prehypertensive Patients

“…Erythrocyte membrane fluidity depends on Na + ,K + -ATPase activity, which is reduced in hypertensive patients [16] and in spontaneously hypertensive rats [6]. The mechanisms underlying such reduction are still obscure, but it has been reported that plasma membrane Na + ,K + -ATPase may be inhibited by ouabain-like endogenous inhibitors [5], which are decreased by physical exercise [17] or antihypertensive agents, which can enhance Na + ,K + -ATPase activity [10]. …”

“…It has been suggested that biochemical and biophysical abnormalities of cell membranes [5] may actively participate in the pathogenesis of hypertension [6], and that such abnormalities seem to be involved not only in vascular smooth muscle cells, but also in circulating blood cells [7]. In fact, it has been reported that viscosity and rigidity of erythrocyte membranes are increased in spontaneously hypertensive rats (SHR) and in patients with essential hypertension [8], and that erythrocyte membrane fluidity depends on Na + ,K + -ATPase activity [6].…”

Enhanced Na+, K+-ATPase activity and endothelial modulation decrease phenylephrine-induced contraction in aorta from ouabain-treated normotensive and hypertensive rats

“…Nevertheless, to our knowledge, this is the first study to investigate the effect of long-term OUA in vascular Na + , K + -ATPase activity in a model of essential hypertension. It was demonstrated that aortic smooth muscle cells from SHRs have diminished Na + , K + -ATPase activity [33]. However, endothelium-derived factors can be released from the aorta of normotensive and SHRs in the presence of OUA, which could activate Na + , K + -ATPase activity [24,34,35].…”