Free Calcium Concentration in Platelets of Patients with Essential Hypertension

Lechi, C.; Bonadonna, Giovanni; Corradini, P.; Polignano, R; Arosio, Enrico; Covi, G; Lechi, Alessandro

doi:10.1159/000167218

Cited by 5 publications

(3 citation statements)

References 10 publications

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“…[11] again observed a slight increase of platelet calcium in essential hyperten sives, but no significant correlation was reported between this and the blood pressure level.…”

Section: Essential Hypertensionmentioning

confidence: 87%

Altered Cellular Calcium Control in Blood Cells in Primary Hypertension

Bruschi¹,

Bruschi²,

Cavatorta³

et al. 1986

Am J Nephrol

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“…[11] again observed a slight increase of platelet calcium in essential hyperten sives, but no significant correlation was reported between this and the blood pressure level.…”

Section: Essential Hypertensionmentioning

confidence: 87%

Altered Cellular Calcium Control in Blood Cells in Primary Hypertension

Bruschi¹,

Bruschi²,

Cavatorta³

et al. 1986

Am J Nephrol

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“…Cellular calcium has been reported to be elevated in red blood cells, vascular smooth muscle cells and platelets of patients with essential hypertension and/or in SHR 5. lo,19,20,32,35. Because blood cells are readily accessible, we studied the lipid metabolism in erythrocytes and platelets of SHR and of patients with essential hypertension. Although it is not known how the intracellular calcium comes to be raised, abnormalities of calcium handling have been convincingly demonstrated in membrane preparations from various cell types in human essential hypertension and in spontaneously hypertensive rats (SHR) 6, 27.…”

Section: Defective Phosphoinositide Metabolism In Primary Hypertensionmentioning

confidence: 99%

“…For an extensive analysis of platelet MAO activity in psychiatric disorders, refer to a recent review by Fowler et al 19. Nevertheless, the platelet has been a useful organelle for the study of basic and clinical actions of psychotropic drugs 34, 44, ~5.…”

Section: Introductionmentioning

confidence: 99%

Defective phosphoinositide metabolism in primary hypertension

et al. 1988

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An increase in free cytosolic calcium content has been reported in essential hypertension. Since within the membrane, the phosphoinositides participate in the control of cell calcium homeostasis, we investigated whether impaired phosphoinositide metabolism could account for the calcium handling abnormality observed in hypertensives. In erythrocyte membranes of hypertensives the activity of kinases involved in polyphosphoinositide formation appears to be impaired and could be related to the alteration in calcium handling binding capacity and ATP-dependent calcium transport. In platelets of hypertensives, the hyperactivity of phospholipase C (observed even in the absence of calcium in the external medium) is likely to be responsible for the hypersensitivity of cells to various agonists. These observations are consistent with the hypothesis that in cells from hypertensives, a membrane defect linked to phosphoinositide metabolism is involved in the overall calcium handling defect.

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Decreased cytosolic calcium and prostaglandin synthesis in prehypertensive rats.

1990

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The capacity of cultured renal medullary interstitial cells derived from Dahl salt-sensitive and salt-resistant rats to synthesize prostaglandin E 2 (PGE 2 ) was compared. Basal and arginine vasopressin (AVP) -induced PGE 2 production by interstitial cells from salt-resistant rats was fourfold to fivefold higher than corresponding values of those from the salt-sensitive rats. Similarly, basal and AVP-responsive release of [ and further supports a role for the interstitial cell as a source of vasodepressor humoral agents. Studies in experimental genetic models of salt-induced hypertension such as the Dahl salt-sensitive (DS) and saltresistant (DR) rat model 5 suggest that inherited differences in the antihypertensive capacity of the renal medulla may explain the differences in the susceptibility of these rats to the development of high blood pressure when they are placed on a high salt diet. Received September 13,1989; accepted in revised form December 11, 1989. Among the factors that have been suggested as contributing to the antihypertensive action of the renal medulla are prostaglandin E2 (PGE2) 6 -9 and antihypertensive polar renomedullary lipid (APRL), 210 a member of a class of lipids, the l-alkyl-2-acylglyceryl-ether phosphorylcholines. The release of arachidonic acid for PGE2 synthesis as well as release of APRL follows activation of cellular lipases and may be triggered by a rise in cytosolic free calcium ([Ca 2+ ]i).u Previous studies in DS and DR rats have demonstrated lower urinary PGE2 excretion and PGE2 content of quick-frozen renal medulla obtained from prehypertensive DS compared with DR rats. 7 -9 The differences in PGE2 persist after the rats are placed on a high salt diet at which point the DS rats become hypertensive, whereas the DR rats remain normotensive. "9 The mechanisms and cell types responsible for this decrease in renal medullary PGE2 production have not been examined in detail. In the present study, we examined 1) the capacity of interstitial cells cultured from the renal medulla of DS or DR rats to synthesize PGE2 basally and in response to vasopressin (AVP), the calcium ionophore A23187, and exogenous arachidonic acid; 2) the relative contribution of

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Free Calcium Concentration in Platelets of Patients with Essential Hypertension

Cited by 5 publications

References 10 publications

Altered Cellular Calcium Control in Blood Cells in Primary Hypertension

Altered Cellular Calcium Control in Blood Cells in Primary Hypertension

Defective phosphoinositide metabolism in primary hypertension

Decreased cytosolic calcium and prostaglandin synthesis in prehypertensive rats.

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