Abnormalities of sodium-magnesium exchange in erythrocytes from essential hypertensive patients

Picado, M. J.; Sierra, A. De La; Aguilera, Mònica; Coca, A.; Pares, I.; Lluch, M.; Sánchez, Muñoz; Urbano-Márquez, Á

doi:10.1097/00004872-199312050-00105

Cited by 3 publications

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“…In essential hypertension, [Cl − ] i in erythrocytes was found to be reduced from 84.4 mmol/l to 70.6 mmol/l [36]. On the other hand, in 45% of patients with essential hypertension, Na + /Mg 2+ antiport was increased [37,38]. In these studies, Na + /Mg 2+ antiport was measured in Mg 2+ ‐loaded erythrocytes, that is under nearly V max conditions of Na + /Mg 2+ antiport.…”

Section: Resultsmentioning

confidence: 77%

Stimulation of Na⁺/Mg²⁺ antiport in rat erythrocytes by intracellular Cl⁻

Ebel

Günther

2003

FEBS Letters

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Section: Resultsmentioning

confidence: 77%

Stimulation of Na⁺/Mg²⁺ antiport in rat erythrocytes by intracellular Cl⁻

Ebel

Günther

2003

FEBS Letters

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“…Although mechanisms underlying alterations in cellular Mg 2+ status in hypertension are unclear, changes in transmembrane Mg 2+ transport could play a role. Previous studies [26,27] have demonstrated hyperactivation of Na + /Mg 2+ exchange activity in hypertension, where Mg 2+ efflux is coupled with Na + influx. We have reported [28] that activity of Na + -dependent Mg 2+ transport is increased in VSMCs from spontaneously hypertensive rats.…”

Section: Introductionmentioning

confidence: 93%

Up-regulation of vascular and renal mitogen-activated protein kinases in hypertensive rats is normalized by inhibitors of the Na+/Mg2+ exchanger

Touyz

Yao

2003

Clinical Science

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In the present in vivo study, we have investigated whether inhibitors of the Na(+)/Mg(2+) exchanger quinidine and imipramine influence the development of hypertension and whether this is associated with modulation of mitogen-activated protein (MAP) kinase activation in arteries and kidneys of hypertensive rats. Sprague-Dawley rats were divided into four groups (n =6/group): control (vehicle), angiotensin II (Ang II; 150 ng/kg of body weight per min subcutaneously), quinidine [Ang II (150 ng/kg of body weight per min)+quinidine (5 mg/kg of body weight per day in food)] and imipramine groups [Ang II (150 ng/kg of body weight per min)+imipramine (5 mg/kg/day in food)]. Rats were studied for 3 weeks. Phosphorylation of vascular and renal extracellular-signal-regulated protein kinase 1/2 (ERK1/2), p38MAP kinase and c-Jun N-terminal kinase (JNK) were assessed using phospho-specific antibodies. Ang II increased systolic blood pressure from 112+/-5 mmHg to 215+/-9 mmHg ( P <0.01). Development of hypertension was attenuated in Ang II-infused rats treated with quinidine (173+/-6 mmHg) and imipramine (152+/-6 mmHg) (P <0.01). Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P <0.05). Activation of renal MAP kinases was also increased in the Ang II group (P <0.05). Quinidine and imipramine reduced the phosphorylation of renal ERK1/2, but did not modify renal p38MAP kinase or JNK. Our data demonstrate that Ang II induces severe hypertension in Sprague-Dawley rats and this is associated with increased phosphorylation of vascular and renal MAP kinases. Quinidine and imipramine attenuated the development of hypertension and normalized MAP kinase activity. The findings from this study suggest a possible role for the Na(+)/Mg(2+) exchanger in vascular signalling events associated with blood pressure elevation in Ang II-dependent hypertension.

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Inhibitors of Na+/Mg2+ exchange activity attenuate the development of hypertension in angiotensin II-induced hypertensive rats

Touyz

Yao

2003

Journal of Hypertension

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Abnormalities of sodium-magnesium exchange in erythrocytes from essential hypertensive patients

Cited by 3 publications

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Stimulation of Na⁺/Mg²⁺ antiport in rat erythrocytes by intracellular Cl⁻

Stimulation of Na⁺/Mg²⁺ antiport in rat erythrocytes by intracellular Cl⁻

Up-regulation of vascular and renal mitogen-activated protein kinases in hypertensive rats is normalized by inhibitors of the Na+/Mg2+ exchanger

Inhibitors of Na+/Mg2+ exchange activity attenuate the development of hypertension in angiotensin II-induced hypertensive rats

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Abnormalities of sodium-magnesium exchange in erythrocytes from essential hypertensive patients

Cited by 3 publications

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Stimulation of Na+/Mg2+ antiport in rat erythrocytes by intracellular Cl−

Stimulation of Na+/Mg2+ antiport in rat erythrocytes by intracellular Cl−

Up-regulation of vascular and renal mitogen-activated protein kinases in hypertensive rats is normalized by inhibitors of the Na+/Mg2+ exchanger

Inhibitors of Na+/Mg2+ exchange activity attenuate the development of hypertension in angiotensin II-induced hypertensive rats

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Stimulation of Na⁺/Mg²⁺ antiport in rat erythrocytes by intracellular Cl⁻

Stimulation of Na⁺/Mg²⁺ antiport in rat erythrocytes by intracellular Cl⁻