Platelet cytosolic proton and free calcium concentrations in essential hypertension

Astarie, C; Levenson, Jaime; Simon, Alain; Meyer, Philippe; Devynck, Marie‐Aude

doi:10.1097/00004872-198906000-00008

Cited by 51 publications

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“…This is in agreement with other studies [17,18]. Although the mecha nism of elevating platelet intracellular cal cium content is not fully understood, Blaustein [19] proposed that a defect in intracellu lar sodium handling might be involved, since it was believed that sodium and calcium in smooth muscle cells of peripheral vascular vessels might be directly interlinked via a sodium/calcium exchange mechanism [20,21], There was no difference in the plasma calcium concentration between the hyperten sive and normotensive groups.…”

Section: Discussionsupporting

confidence: 90%

Are Platelet Cytosolic Free Calcium, Serotonin Concentration and Blood Viscosity Different between Hypertensive and Normotensive Subjects?

Ding¹,

Chou

Huan³

1994

Cardiology

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In this study, the platelet intracellular calcium and serotonin (5-HT) concentrations as well as the hemorheological properties were compared in 65 hypertensive (HT) and 25 age-matched normotensive (NT) subjects. The result showed that the platelet intracellular calcium concentration in the HT group was significantly higher than in the NT group (165.4 ± 12.6 vs. 118.9 ± 12.4 nM, p < 0.05). However, the platelet 5-HT content in the HT group was significantly lower than in the NT group (0.28 ± 0.03 vs. 0.38 ± 0.03 nmol/10⁸ platelets, p < 0.05). Moreover, red cell flexibility, red cell deformability, hematocrit, fibrinogen concentration and plasma viscosity were all significantly increased in HT subjects. The whole blood viscosity was generally higher in the HT group. In conclusion, the higher platelet intracellular calcium and lower 5-HT level as well as abnormality of hemorheological properties may be important factors in the initiation and perpetuation of hypertension.

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Section: Discussionsupporting

confidence: 90%

Are Platelet Cytosolic Free Calcium, Serotonin Concentration and Blood Viscosity Different between Hypertensive and Normotensive Subjects?

Ding¹,

Chou

Huan³

1994

Cardiology

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“…Determinations of plat 9 calcium concentrations in primary hypertension [1,6,9,13,20,21,23,28,29], hypertension of chronic renal failure [31], and preeclampsia [17,18, 37] using quin 2 or fura 2 have also revealed increased intracellular free-calcium concentrations. These investigators also obtained significant correlations between blood pressure or vascular resistance and intracellular calcium concentration in platelets.…”

Section: Discussionmentioning

confidence: 99%

Modulation of platelet Ca2+ homeostasis by hypertensive plasma factor(s) derived from patients with early-stage renal disease

Schiffl

1991

Klin Wochenschr

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To determine whether blood-borne factors in hypertension accompanying early-stage kidney disease might be responsible for altered cellular calcium homeostasis, we measured changes in cytosolic calcium before and after incubating platelets in plasma ultrafiltrates from normotensive and hypertensive renal patients. With the use of the chelating agent quin 2, we found the free-calcium concentrations in platelets to be higher in the hypertensive than in the normotensive group. When both groups of participants were combined, a direct correlation was found between arterial pressure and cytosolic calcium. The cytosolic calcium concentration in platelets of normotensive renal patients increased after incubation with plasma from patients with untreated renal hypertension, but it was unchanged after incubation with plasma from normotensive subjects. These data indicate that the total cell burden of calcium is increased in platelets of hypertensive patients with early-stage renal disease, and that plasma from these patients contains a substance that is capable of increasing the cytosolic calcium concentration in platelets. If the plasma factor (or factors) acts not only on platelets, but also on vascular smooth muscle cells, it may contribute to the increased peripheral vascular resistance associated with hypertension of renal origin.

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“…In contrast, Ng and co-workers reported that leucocytes from Ht patients were significantly more alkaline than those from Nt subjects [16] whereas more recently no difference in leucocytes and skeletal muscle pHi between Nt and Ht subjects was described [19]. In their study on platelets, Astarie et al [36] claimed that pHi was higher in cells from Ht donors when compared to Nt controls. On the contrary, no difference could be demonstrated in platelets from Ht and Nt by Tokudome et a/.…”

Section: Activity Of Na+/h+ Antiport In Hypertensive Subjectsmentioning

confidence: 94%

The lymphocyte Na⁺/H⁺ antiport: activation in primary hypertension and during chronic NaCl‐loading

Göbel

Hoffmann

Ruppert

et al. 1994

Eur J Clin Investigation

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Increased activity of the Na+/H+ antiport may be a major abnormality in essential hypertension. The activity of this transport system was investigated in lymphocytes from 13 patients with untreated essential hypertension (Ht) and 13 normotensive control subjects (Nt) on an ad libitum (130-170 mmol d-1) NaCl intake. Furthermore, the effects of different states of NaCl balance on lymphocyte Na+/H+ antiport were evaluated in two groups of Nt volunteers receiving 20 vs. 300 mmol d-1 (n = 8) and 85 vs. 200 mmol d-1 (n = 14) of NaCl for 1 week each and in seven Ht patients (20 vs. 300 mmol NaCl d-1 for 1 week each). Additionally, during the 20 and 300 mmol/d NaCl intake red blood cell membrane transport was studied in eight subjects. For the determination of lymphocyte antiport activity, cells were loaded with the cytosolic pH (pHi) indicator bis-carboxyethyl carboxyfluorescein (BCECF-AM) and acidified by addition of different amounts of Na(+)-propionate (5-40 mM). Initial pHi-recovery was taken as the activity of the antiport system and plotted against pHi-values after acidification. Non-linear regression analysis yielded higher 'apparent' maximal transport rates in Ht than Nt (Nt: 2.00 +/- 0.22; Ht: (3.81 +/- 0.59) x 10(-3) s-1; P < 0.025). In contrast, baseline pHi-values and pHi-values at half-maximal activity (pK) were identical in Nt and Ht. In normotensive control subjects on an NaCl intake of 20, 85, 200 and 300 mmol d-1 for 7 d, 'apparent' maximal transport rates averaged 2.75 +/- 0.20, 2.89 +/- 0.17, 2.81 +/- 0.18 and (3.62 +/- 0.25) x 10(-3) s-1, respectively. Thus, antiport activity was significantly (P < 0.05) stimulated on the 300 mmol d-1 intake as compared to the three other NaCl intakes. The extreme intakes of NaCl (20 vs. 300 mmol d-1) in normotensive volunteers did not affect the erythrocyte Na+/K+ pump, Na+/K+ cotransport and Na+/Li+ countertransport. Our study supports the concept that a group of patients with primary hypertension exhibit an activated Na+/H+ antiport. Furthermore, our data demonstrate that a chronic high intake of NaCl is associated with an increase in lymphocyte antiport activity towards the high values observed in primary hypertension.

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Platelet cytosolic proton and free calcium concentrations in essential hypertension

Cited by 51 publications

References 0 publications

Are Platelet Cytosolic Free Calcium, Serotonin Concentration and Blood Viscosity Different between Hypertensive and Normotensive Subjects?

Are Platelet Cytosolic Free Calcium, Serotonin Concentration and Blood Viscosity Different between Hypertensive and Normotensive Subjects?

Modulation of platelet Ca2+ homeostasis by hypertensive plasma factor(s) derived from patients with early-stage renal disease

The lymphocyte Na⁺/H⁺ antiport: activation in primary hypertension and during chronic NaCl‐loading

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Platelet cytosolic proton and free calcium concentrations in essential hypertension

Cited by 51 publications

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Are Platelet Cytosolic Free Calcium, Serotonin Concentration and Blood Viscosity Different between Hypertensive and Normotensive Subjects?

Are Platelet Cytosolic Free Calcium, Serotonin Concentration and Blood Viscosity Different between Hypertensive and Normotensive Subjects?

Modulation of platelet Ca2+ homeostasis by hypertensive plasma factor(s) derived from patients with early-stage renal disease

The lymphocyte Na+/H+ antiport: activation in primary hypertension and during chronic NaCl‐loading

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The lymphocyte Na⁺/H⁺ antiport: activation in primary hypertension and during chronic NaCl‐loading