Platelet volume responses to cytoplasmic acidification in essential hypertension

Weder, Alan B.; Schmouder, Robert; Torretti, Barbara A.

doi:10.1097/00004872-199012000-00010

Cited by 7 publications

(8 citation statements)

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“…The mechanisms involved in swelling of platelets upon exposure to an acidic Na ÷ propionate medium have been investigated in detail [10, 26,40]. The main process consists of an uptake of uncharged propionic acid into the cytosol where protons dissociate, thereby causing intracellular acidification.…”

Section: Discussionmentioning

confidence: 99%

“…The continuing ion exchange finally raises intracellular Na ÷, thereby increasing the intracellular osmotically active ion concentration. The uptake of osmotically obliged water results in cell swelling which can be determined by electronic cell sizing [10,40]. In our previous report we demonstrated that addition of platelets to Na ÷ propionate medium induces a decrease in light absorption of platelet suspensions [26].…”

Section: Discussionmentioning

confidence: 99%

“…Hence the enduring acidification leads to an osmotically effective rise in intracellular Na ÷ which finally results in cell swelling. The velocity of the increase in cell volume can be quantified by electronic cell sizing using a Coulter Counter as originally proposed by Grinstein's group [10], and the same technique has been successfully applied to demonstrate an enhanced Na ÷/H ÷ exchange activity in platelets and lymphocytes of patients with EH [17,30,40,41]. In the present study we utilized a modification of the aforementioned technique details of which were described only recently [26].…”

Section: Determination Of Platelet Antiport Activitymentioning

confidence: 99%

“…This activates the Na+/H ÷ exchanger which extrudes protons in exchange for extracellular sodium. In the presence of a large amount of extracellular propionic acid continuing to permeate into the cells, persistent activation of the Na ÷/H ÷ exchanger results in an increase in intracellular sodium and thus osmolality and in cell swelling due to the inward osmotic gradient [40].…”

Section: Determination Of Platelet Antiport Activitymentioning

confidence: 99%

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Platelet Na+/H+ antiport activity in patients with insulin-dependent diabetes mellitus with and without diabetic nephropathy

et al. 1993

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The incidence of diabetic nephropathy in patients with insulin-dependent diabetes mellitus (IDDM) may depend on factors other than the quality of diabetes control. Hypertension is an additional factor associated with a high degree of renal involvement in IDDM. One abnormality consistently observed in various tissues of patients with essential hypertension is enhanced activity of the Na+/H+ antiport. In the present study we have therefore studied platelet antiport activity in 41 healthy subjects (control), in 22 patients with untreated essential hypertension (EH), and in 35 normotensive IDDM patients (type 1). Of these patients 17 exhibited signs of diabetic nephropathy (group 1) while 18 had no evidence for renal involvement of IDDM in spite of a duration of IDDM of at least 10 years (group 2). The two IDDM patient groups were undistinguishable with respect to age, body mass index, and arterial blood pressure (group 1, 117.9 +/- 2.4/78.4 +/- 1.5 mmHg; group 2, 113.9 +/- 3.6/76.1 +/- 1.8 mmHg). Antiporter activity was determined from the rate of cell volume changes induced by propionic acid. Platelet Na+/H+ exchange activity averaged 23.43 +/- 0.43 10(-3).s-1 in control subjects and was markedly elevated in EH (28.38 +/- 0.62 10(-3).s-1; P < 0.01). Antiport activity in group 2 patients without nephropathy averaged 24.54 +/- 0.57 10(-3).s-1 and was undistinguishable from the control group. However, platelet Na+/H+ antiport activity was significantly stimulated in group 1 patients with nephropathy as compared to group 2 (26.95 +/- 0.73 10(-3). s-1; P < 0.025). Our results show that renal involvement in IDDM is associated with enhanced activity of the platelet Na+/H+ antiport.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Determination Of Platelet Antiport Activitymentioning

confidence: 99%

Section: Determination Of Platelet Antiport Activitymentioning

confidence: 99%

See 2 more Smart Citations

Platelet Na+/H+ antiport activity in patients with insulin-dependent diabetes mellitus with and without diabetic nephropathy

et al. 1993

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“…However, a long follow-up study would be necessary to ascer tain the validity of this supposition. 16 Agam/Deutsch/Karplus/Livne Li'-Na* Countertransport…”

Section: Discussionmentioning

confidence: 99%

Erythrocyte Li+i-Na+o Countertransport in the Newborn

Agam

Deutsch²,

Karplus³

et al. 1993

Neonatology

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The present study investigates the erythrocyte Li_i⁺-Na_o⁺ countertransport (CT) in the newborn. Erythrocytes of term infants exhibit no or very low CT activity at birth (0.025 ± 0.011 mmol Li/1 RBC·h). CT rates increase gradually and reach adult values within the 4th-7th day of life (0.225 ± 0.018 mmol Li/1 RBC·h). CT activity in healthy preterm infants at birth is not significantly different from that in term infants (0.014 ± 0.007 mmol Li/1 RBC·h). Postnatal maturation of CT activity in preterm infants is similar to that found in term infants and is independent of gestational age. However, CT rates at birth of premature infants subjected to prenatal stress are significantly higher (0.082 ± 0.017 mmol Li/1 RBC·h). It is concluded that erythrocyte CT activity in the newborn reaches adult values within the first week of life, apparently reflecting the postnatal maturation of the CT system in the cell membrane. We suggest that prenatal stress induces the synthesis of the CT protein in utero.

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Plasma lipids affect maximum velocity not sodium affinity of human sodium‐lithium countertransport: distinction from essential hypertension

Rutherford

Thomas

Laker

et al. 1992

Eur J Clin Investigation

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Inheritance is a major determinant of increased sodium-lithium countertransport (SLC) activity in hypertension. However, hyperlipidaemia can also cause increased SLC activity in some individuals and it is difficult to distinguish this effect from the effect of hypertension. Erythrocyte SLC activity and its kinetic determinants sodium affinity (km) and maximum velocity (Vmax) were measured in 25 hyperlipidaemic patients and 15 normal controls (NC). Increased SLC activity (0.31 +/- SEM 0.03 mmol Li/(h x 1 cells) vs. NC 0.20 +/- 0.01, P < 0.01) in the hyperlipidaemic patients was associated with increased Vmax (0.59 +/- 0.07 vs. NC 0.41 +/- 0.03, P < 0.01) but normal km (median 120 range [40-324] mmol l-1 vs. 140 [108-260]. Lipid-lowering therapy resulted in decreased SLC activity secondary to a fall in Vmax. Km remained constant despite the changes in lipids and Vmax. The mechanism of increased SLC activity in hyperlipidaemia is different from that in essential hypertension where increased sodium affinity is found. Measurement of the kinetic characteristics of SLC may discriminate between the independent influences of hypertension and hyperlipidaemia on the sodium-lithium countertransporter.

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Platelet volume responses to cytoplasmic acidification in essential hypertension

Cited by 7 publications

References 0 publications

Platelet Na+/H+ antiport activity in patients with insulin-dependent diabetes mellitus with and without diabetic nephropathy

Platelet Na+/H+ antiport activity in patients with insulin-dependent diabetes mellitus with and without diabetic nephropathy

Erythrocyte Li<sup>+</sup><sub>i</sub>-Na<sup>+</sup><sub>o</sub> Countertransport in the Newborn

Plasma lipids affect maximum velocity not sodium affinity of human sodium‐lithium countertransport: distinction from essential hypertension

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