Decreased membrane Mg2+ concentrations in a subgroup of hypertensives☆Membrane model for the pathogenesis of primary hypertension

Kisters, Klaus; Tepel, Martín; Spieker, C.; Zidek, Walter; Barenbrock, Michael; Tokmak, Faruk; Kosch, Markus; Hausberg, Martin; Rahn, K. H.

doi:10.1016/s0895-7061(98)00169-1

Cited by 31 publications

(12 citation statements)

References 14 publications

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“…19 We could recently demonstrate significantly decreased membrane Mg ++ concentrations in a subgroup of patients with essential hypertension. 10 However, these parameters were not measured in the present study and contribution of the mentioned factors remains speculative.…”

Section: Discussionmentioning

confidence: 66%

“…Erythrocyte and plasmalemmal membrane preparations were performed as described elsewhere. 10 Briefly, erythrocytes were washed three times by sedimenting in a swinging-bucket rotor (2300 g for 10 min) and the pellet resuspended in 5 mmol/l phosphate buffered saline (150 nmol/l sodium chloride and 5 mmol/l sodium phosphate, pH 8.0). The buffy coat was carefully aspirated each time from the surface of the pellet.…”

Section: Calcium Measurementsmentioning

confidence: 99%

“…After two more identical cycles the ghost membranes were creamy white and morphologically intact based on previous investigations and on optical control. 10 The Ca ++ contents were then determined by atomic spectroscopy and referred to membrane protein content. The measurements of protein content were performed using Coomassie Blue (Serva, Deisenhofen, Germany) according to Bradford's method.…”

Section: Calcium Measurementsmentioning

confidence: 99%

“…In humans, increased cytosolic calcium concentrations in platelets and erythrocytes have been described, although data are equivocal. 2,[5][6][7][8][9][10] Additionally, animal data suggest disturbed membrane calcium handling in hypertensive rats. 11 Calcium influx across the external cellular membrane in smooth muscle cells and cardiomyocytes plays a crucial role in the control of cellular excitation, contraction and impulse propa- gation.…”

Section: Introductionmentioning

confidence: 99%

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Increased membraneous calcium concentrations in primary hypertension: a causal link to pathogenesis?

et al. 2000

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Background: Disturbance in calcium metabolism has been suggested in the pathogenesis of hypertension, however, membrane calcium content in humans has not been studied in detail yet in primary hypertension. We compared plasma, intracellular and membrane calcium concentrations in erythrocytes of patients with essential hypertension and in healthy, normotensive control subjects to determine a possible alteration of membrane calcium in primary hypertension. Subjects and Methods: Thirty-four never treated patients with essential hypertension were included and 34 healthy, age-and sex-matched volunteers served as controls. Atomic absorption spectroscopy was used for measurement of intracellular and membrane calcium content in erythrocytes and plasmalemmal preparations. Results: Plasma and intracellular Ca ++ concentrations

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Section: Discussionmentioning

confidence: 66%

Section: Calcium Measurementsmentioning

confidence: 99%

Section: Calcium Measurementsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Increased membraneous calcium concentrations in primary hypertension: a causal link to pathogenesis?

et al. 2000

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“…In this context changes in magnesium metabolism have been implicated in the pathogenesis of hypertension [9,10,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,36] Therefore it was of interest to study magnesium deficient patients with essential hypertension concerning CIMT.…”

Section: Introductionmentioning

confidence: 99%

Magnesium metabolism and cardiovascular diseases

Kisters¹,

Al-Tayar²,

Nguyen³

et al. 2011

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A magnesium defieieney is known to be involved in the pathogenesis of primary hypertension. In patients with essential hypertension intima media thickness is increased in about 70% (ELSA Study), In our study, we investigated 21 patients ( 10 female, 11 male, average age 56.3 ± 6,6 years) with untreated essential hypertension (Grades I and II according to WHO guidelines). All patients had a hypomagnesemia in serum (1,57 ±0.11 mg%). In all patients we found a significant increase in intima media thickness of arteria carotis communis (0,97 ± 0,08 mm) (r =-0.869, p< 0.0001). The results show that a magnesium defieieney in' patients with essential hypertension may be of speeial pathogenetie importance. In addition, the role of magnesium deficiency in the development of arteriosclerosis has to be diseussed. Furthermore, we demonstrated a eonnection between magnesium defieieney and an inereased intima media thickness. In this context, calcium antagonist therapy or magnesium supplementation may be of' advantage when treating intima media thickness in hypertension.

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Lowered total intracellular magnesium status in a subgroup of hypertensives

et al. 2011

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A new method to determine total Mg++ content in lymphocytes was developed, offering advantages for routine measurements as compared to fluorescence methods. Intracellular total Mg++ measurements were performed in lymphocytes of 18 healthy subjects and 19 untreated essential hypertensive patients. Mg++ content was referred to lymphocytic and membrane protein, which was determined according to Bradford's method. Mg++ measurements were performed by atomic absorption spectroscopy using a Video 12 apparatus of Thermo Electron Instrumentation Laboratory, Andover, USA. The results show that in patients with essential hypertension total intralymphocytic Mg++ content is significantly lower (0.07 +/- 0.05 mmol/g lymphocytic protein, mean +/- s.d.) as compared to controls (0.11 +/- 0.04 mmol/g lymphocytic protein, mean +/- s.d., p < 0.05). Free intracellular Mg++ content was measured in lymphocytes by the fluorescent indicator mag-fura-II, showing no significant differences in normotensives and hypertensives (0.30 +/- 0.16 versus 0.38 +/- 0.17 mmol/l). Additionally, in platelets free intracellular Mg++ concentrations were not found of significant difference in normotensives and hypertensives (0.52 +/- 0.23 versus 0.47 +/- 0.27 mmol/l) using mag-fura-II. In plasma Mg++ concentrations there was no significant difference in the normotensive and hypertensive group (0.92 +/- 0.07 versus 0.88 +/- 0.07 mmol/l). There was no correlation between plasma or free or total cellular magnesium concentrations in both groups. Furthermore this method seems also suitable for routine measurements of total intracellular Mg++ concentrations in even larger measurements like mag-fur-II. Lowered total intracellular Mg++ concentrations in a subgroup of primary hypertensives may contribute to the development of this disorder, perhaps due to different buffering systems.http://link.springer-ny.com/link/service/journals/00547/bibs/8n3p154.html

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Decreased membrane Mg2+ concentrations in a subgroup of hypertensives☆Membrane model for the pathogenesis of primary hypertension

Cited by 31 publications

References 14 publications

Increased membraneous calcium concentrations in primary hypertension: a causal link to pathogenesis?

Increased membraneous calcium concentrations in primary hypertension: a causal link to pathogenesis?

Magnesium metabolism and cardiovascular diseases

Lowered total intracellular magnesium status in a subgroup of hypertensives

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