Platelet membrane calmodulin-stimulated calcium-adenosine triphosphatase. Altered activity in essential hypertension.

Resink, Thérèse J.; Ткачук, В. А.; Erné, Paul; Bühler, Fritz R.

doi:10.1161/01.hyp.8.2.159

Cited by 63 publications

(22 citation statements)

References 32 publications

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“…The Na+/Ca2" exchanger and the Ca2+-ATPase systems are present in VSMC to maintain a positive Ca2" gradient (40)(41)(42)(43). Insulin stimulates Ca2"-ATPase activity in dog and rat kidney basolateral membranes (18,44 (50).…”

Section: Methodsmentioning

confidence: 99%

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

Saito¹,

Hori²,

Fittingoff³

et al. 1993

J. Clin. Invest.

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Insulin has been shown to attenuate pressor-induced vascular contraction, but the mechanism for this vasodilatory action is unknown. This study examines the effect of insulin on angiotensin II (ANG II)-induced increments in cytosolic calcium in cultured rat vascular smooth muscle cells (VSMC). 20-min incubations with insulin (10 ,U/ml to 100 mU/ml) did not alter basal intracellular calcium concentration (ICa2I,), but inhibited the response to 100 nM ANGII in a dose-dependent manner (ANG II alone, 721±54 vs. ANG II + 100 mU/ml insulin, 315±35 nM, P < 0.01). A similar effect of insulin on ANGII action was observed in calcium poor buffer. Moreover, insulin did not effect calcium influx. ANG II receptor density and affinity were not affected by 24-h incubation with insulin. To further clarify the mechanisms of these observations, we measured ANG II-induced production of inositol 1,4,5-triphosphate (IP3), and IP3-releasable 45Ca. Insulin treatment did not alter ANG Il-stimulated IP3 production. However, IP3-stimulated release of45Ca in digitonin permeabilized cells was significantly reduced after 5-min incubations with 100 mU/ml insulin. Thapsigargin induced release of calcium stores was also blocked by insulin. Thus, insulin attenuates ANG 11-stimulated ICa2"I, primarily by altering IP3-releasable calcium stores. Insulin effects on ANG II-induced ICa2`Ii were mimicked by preincubation of VSMC with either sodium nitroprusside or 8-bromo-cGMP. As elevations in cGMP in vascular tissue lower ICa2I1j, it is possible that insulin affects IP3 release of calcium by a cGMP-dependent mechanism that would contribute to its vasodilatory effects. (J. Clin. Invest. 1993. 92:1161-1167

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Section: Methodsmentioning

confidence: 99%

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

Saito¹,

Hori²,

Fittingoff³

et al. 1993

J. Clin. Invest.

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“…43 Thus, fibroblasts from blacks appear to have a higher calcium turnover rate than those from whites, and the same phenomenon may also be present in their platelets. Resink et al 45 have suggested a similar process with regard to platelets of essential hypertensive subjects by demonstrating higher activities of both the calmodulin-sensitive and calmodulin-insensitive components of calcium ATPase in these cells. This observation could not be confirmed by our group.…”

mentioning

confidence: 86%

Variations in the apparent pH set point for activation of platelet Na-H antiport.

et al. 1990

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To explore the role of the Na-H antiport in essential hypertension, we studied the kinetics of cytosolic pH and external sodium activation of this transport system in platelets from 65 normotensive and essential hypertensive subjects on and off antlhypertensive medications. Subjects included both blacks and whites, as well as men and women. The fluorescent dye 2'7-bis(carboxyethyl)-5,6-carboxyfluorescein was used to monitor the cytosolic pH in these cells. Platelets from black (hypertensive and normotensive) men and hypertensive white men demonstrated a highly significant alkaline shift in the apparent cytosolic pH set point for activation of the Na-H antiport. For the hypertensive subgroups, the cytosolic pH set point values (mean±SEM) were: white men, 7.45 ±0.052; white women, 7.04 ±0.089; black men, 7.66±0.148; and black women, 7.20±0.082. For the normotensive subgroups, the cytosolic pH set point values were: white men, 7.13 ±0.034; white women, 7.05 ±0.036; black men, 7.50±0.110; and black women, 7.20±0.176 (p=0.0016 for race and/>=0.0001 for gender, using a three-way analysis of variance by race, gender, and hypertension). There were no race-, gender-, or blood pressure-related differences among the various cohorts in the kinetics of sodium activation of the Na-H antiport, the cellular buffering power, and basal pH. These results suggest that at basal pH the Na-H antiport is quiescent in platelets from both black and white women and normotensive white men. However, it can be active at basal pH in platelets from black men (normotensive and hypertensive) and in platelets from hypertensive white men. Our work demonstrates the heterogenous nature of the alterations in the Na-H antiport in essential hypertension and its dependence on gender and racial extraction. (Hypertension 1990;16:180-189) T he current consensus holds that alterations in the cellular regulation of cytosolic free calcium (Caj) and cytosolic sodium (Naj) participate in the pathophysiology of essential hypertension. This concept has emerged from numerous studies demonstrating that several ion transport systems are altered in this disease. Recently, the focus of a number of investigations has been on human platelets, inasmuch as these circulating cells are responsive to a variety of agonists that regulate Caj and Naj. Moreover, platelets share characteristics with vascular smooth muscle cells, which play an important role in the increased peripheral vascular resistance that occurs in essential hypertension. One

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“…20 The latter phenomenon was also observed in plasma membranes of cardiomyocytes and adipocytes of SHR, 13 and an increase of intracellular exchangeable calcium was revealed in adipose tissue in both types of primary hypertension. 27 At the same time, decreased activity of the calmodulin-dependent component of calcium pump activity was revealed in erythrocytes 28 and platelets 29 of EH patients and in erythrocytes, 30 synaptosomes, 25 and cardiomyocytes 31 of SHR. These studies were followed up by the finding of increased cytoplasmic free calcium concentration in platelets of both EH patients 32 The relation between alterations of cell calcium homeostasis and abnormalities in the transport systems of univalent cations in the plasma membrane is not always sufficiently clear.…”

mentioning

confidence: 89%

An approach to the explanation of cell membrane alteration in primary hypertension.

Postnov¹

1990

Hypertension

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Platelet membrane calmodulin-stimulated calcium-adenosine triphosphatase. Altered activity in essential hypertension.

Cited by 63 publications

References 32 publications

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

Variations in the apparent pH set point for activation of platelet Na-H antiport.

An approach to the explanation of cell membrane alteration in primary hypertension.

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