Control of the erythrocyte free Ca2+ concentration in essential hypertension.

David‐Dufilho, Monique; Astarie, C; Pernollet, Marie-Gabrielle; Pino, Muriel Del; Levenson, Jaime; Simon, Alain; Devynck, Marie‐Aude

doi:10.1161/01.hyp.19.2.167

Cited by 53 publications

(20 citation statements)

References 39 publications

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“…The increased Na + -H + exchange activity might not be determined only by the hyperinsulinemic state but also by the synergic interaction with cytosolic Ca 2+ , another antiporter modulator, which has been reported to have elevated values in RBCs of hypertensive patients. 48 In summary, our studies reveal that increased Na + -H + exchange activity as measured in RBCs is present in black hypertensive subjects with insulinresistant glucose disposal. Our results also demonstrate that despite impaired insulin-mediated glucose disposal in hypertensive subjects, the cellular Na + gain via enhanced activity of Na + -H + exchange is not blunted.…”

mentioning

confidence: 56%

Red blood cell sodium-proton exchange in hypertensive blacks with insulin-resistant glucose disposal.

1993

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To define the potential pathogenic role of hyperinsulinemia as a mediator of alterations in sodium transport, we have examined red blood cell Na(+)-H+ and Na(+)-Li+ exchanges in a young adult black population characterized for blood pressure and insulin-mediated glucose disposal. Normotensive and mildly hypertensive blacks (blood pressure, 120 +/- 2/76 +/- 2 and 139 +/- 3/94 +/- 2 mm Hg, respectively) with a mean age of 26.1 years were studied for insulin sensitivity with the euglycemic hyperinsulinemic clamp (molar index of insulin sensitivity, M/I = moles glucose metabolized/insulin in milliliters of plasma). Na(+)-H+ exchange (U = mmol/L cell.h) was measured before and after the insulin clamp as a function of cell pH to determine the maximum transport rate. In the normotensive subjects, 18 were insulin sensitive (M/I = 9.37 +/- 0.6 x 10(4)) and 4 were insulin resistant (M/I = 3.64 +/- 0.6 x 10(4)). In the hypertensive subjects, 4 were insulin sensitive (M/I = 9.15 +/- 1.1 x 10(4)) and 16 were insulin resistant (M/I = 3.02 +/- 0.3 x 10(4)). The maximum rate of Na(+)-H+ exchange was significantly higher in all hypertensive vs normotensive individuals (35 +/- 3 vs 23 +/- 3 U, P < .005). Na(+)-H+ exchange activity was higher in insulin-resistant vs insulin-sensitive hypertensive subjects (40 +/- 3 vs 20 +/- 2 U, P < .001) but not in insulin-resistant normotensive subjects. Na(+)-Li+ exchange was not different in hypertensive and normotensive individuals but was higher in all insulin-resistant compared with all insulin-sensitive subjects (0.26 +/- 0.03 vs 0.16 +/- 0.02 U, P < .01). Na(+)-Li+ exchange also was higher in insulin-resistant vs insulin-sensitive normotensive subjects (0.35 +/- 0.03 vs 0.15 +/- 0.02 U, P < .001) and in insulin-resistant hypertensive subjects vs insulin-sensitive normotensive subjects (0.24 +/- 0.03 vs 0.15 +/- 0.02 U, P < .001). A stepwise multiple regression analysis for all variables revealed that with Na(+)-H+ exchange as a dependent variable the main determinant was blood pressure, which in turn had insulin sensitivity as the main determinant. In conclusion, these results indicate that in hypertensive blacks, insulin-resistant glucose disposal is strongly associated with elevated red blood cell Na(+)-H+ exchange activity. Thus, despite impaired insulin-mediated glucose disposal, cellular Na+ gain via enhanced activity of Na(+)-H+ exchange is not blunted in hypertensive blacks.

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confidence: 56%

Red blood cell sodium-proton exchange in hypertensive blacks with insulin-resistant glucose disposal.

1993

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“…32 Furthermore, it has been reported that an accumulation of calcium inside the erythrocyte may lead to changes in cytoskeletal conformation and viscoelasticity of the membrane, so the cells would become less deformable. 33,34 Another original finding of our study was the lack of difference in erythrocyte sialic acid content between normotensive and hypertensive subjects, whereas hypercholesterolemia was associated with decreased erythrocyte sialic acid content in both normotensive and hypertensive groups compared with subjects with low cholesterol. The observation of similar levels of membrane sialic acid content in both hypertensive and normotensive groups was in good agreement with the literature data reporting that total sialic acid content in erythrocyte membrane did not differ between normotensive patients and those with essential or renal hypertension.…”

Section: Hadengue Et Al August 1998mentioning

confidence: 75%

Erythrocyte Disaggregation Shear Stress, Sialic Acid, and Cell Aging in Humans

et al. 1998

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Abstract-Erythrocyte aggregation, which plays an important role in the physiological behavior of blood fluidity, was found to be enhanced in hypertension and hypercholesterolemia. While the role of macromolecule bridging force has been widely described, cellular factors related to membrane sialic acid content, which might contribute to the negative charge of cell surface causing the repulsion of erythrocytes, have been less studied. Cell age-dependent changes in membrane sialic acid content (in micromoles per gram of integral membrane protein) were investigated in 24 normotensive and 24 hypertensive matched subjects, each divided into 2 identical subgroups according to a cutoff of 6.2 mmol/L serum cholesterol. A progressive and significant (PϽ0.001) decrease in membrane sialic acid content associated with an increase (PϽ0.001) of disaggregation shear rate threshold (laser reflectometry in the presence of dextran) were observed with increased erythrocyte density (erythrocytes fractionated by density using ultracentrifugation) in both normotensive and hypertensive groups regardless of the cholesterol level. However, disaggregation shear rate threshold was significantly higher and sialic acid content was lower (PϽ0.001) in both hypertensive and normotensive subjects with hypercholesterolemia compared with either normotensive or hypertensive subjects with low cholesterol, respectively. A high membrane sialic acid content variance, beginning in the younger erythrocytes, was due mainly to triglyceride and LDL cholesterol levels (R 2 ϭ0.49 for low, R 2 ϭ0.43 for middle, and R 2 ϭ0.54 for high densities, ie, young, mean, and senescent erythrocytes, respectively). We conclude that an early decrease in erythrocyte sialic acid content may influence the rheological properties of blood by increasing the adhesive energy of erythrocyte aggregates. (Hypertension. 1998;32:324-330.) Key Words: erythrocyte aggregation Ⅲ rheology Ⅲ sialic acid Ⅲ hypertension, essential Ⅲ hypercholesterolemia E rythrocyte aggregation is one of the main determinants influencing blood circulation at low shear rates by increasing blood viscosity and inducing "sludging" in the capillary.1 Aggregation of red blood cells is a reversible process that occurs when the bridging force due to the adsorption of macromolecules onto adjacent cell surfaces exceeds the disaggregation forces caused by electrostatic repulsion, membrane strain, and mechanical shearing. [1][2][3] An increase in erythrocyte aggregation was found to be associated with cardiovascular risk factors such as hypertension, 4 hyperlipoproteinemia, 5,6 and smoking 7 and in clinical situations such as myocardial ischemia, 8 thromboembolic states, 9 and retinal venous occlusion. 10 In general, most studies have focused on the ability of plasma proteins and various polymers to induce erythrocyte aggregation. We showed that in hypertension and hypercholesterolemia the increase in erythrocyte aggregation could be attributed to an increase in the concentration of plasma fibrinogen. 4,6 In addition, in ...

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“…38 Moreover, absolute peripheral blood flow is reduced in human hypertension 39 because of high blood viscosity 40 and abnormal erythrocyte rheology, such as reduced membrane fluidity, 41 and an elevated erythrocyte free Ca 2+ concentration. 42 This line of evidence implies that circulating erythrocytes of hypertensive patients experience persistent inflammatory damage and shear stress, which impairs erythrocyte filterability by signal transduction involving intracellular Ca 2+ . This can affect the blood's rheologic properties and the interaction of erythrocytes and resistance vessels, contributing to the elevation in flow resistance and BP.…”

Section: Discussionmentioning

confidence: 99%

Impaired Erythrocyte Filterability of Spontaneously Hypertensive Rats: Investigation by Nickel Mesh Filtration Technique

Ariyoshi

Maruyama

Odashiro

et al. 2010

Circ J

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Control of the erythrocyte free Ca2+ concentration in essential hypertension.

Abstract: Since Ca2+ ions seem to directly participate in the control of erythrocyte membrane structure and deformability and because cell Ca 2+ metabolism has been repeatedly proposed to be modified in hypertension, the intracellular calcium ion concentration (

Cited by 53 publications

References 39 publications

Red blood cell sodium-proton exchange in hypertensive blacks with insulin-resistant glucose disposal.

Red blood cell sodium-proton exchange in hypertensive blacks with insulin-resistant glucose disposal.

Erythrocyte Disaggregation Shear Stress, Sialic Acid, and Cell Aging in Humans

Impaired Erythrocyte Filterability of Spontaneously Hypertensive Rats: Investigation by Nickel Mesh Filtration Technique

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