Platelet Membrane and Calcium Control Abnormalities in Essential Hypertension

Fr, Bühler; Tj, Resink

doi:10.1093/ajh/1.1.42

Cited by 27 publications

(7 citation statements)

References 19 publications

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“…Indeed, an increase in cytosolic calcium concentration is a major signal underlying platelet activation. [92][93][94] This is mediated via calcium channels that open mainly in response to "classic" agonist receptors such as adrenaline, thrombin, and ADP, 95,96 although the major receptor concerned with calcium transport is the ionotrophic P 2XI purinoreceptor. 97 Further evidence of the possible involvement of the calcium ion in hypertension include reports of its correlation with blood pressure and reduction with successful treatment.…”

Section: Calcium Channel Blockersmentioning

confidence: 99%

Pharmacological Modulation of Platelet Function in Hypertension

2003

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Abstract-Platelets exert a considerable influence on human morbidity and mortality. The rationale for their study in hypertension follows the observation that the major consequences of hypertension are stroke and myocardial infarction. However, the etiology of these consequences in hypertension is, paradoxically, not hemorrhagic (as might be expected from the effects of high blood pressure), but occlusive, with thrombus being the culprit lesion. Mechanisms of platelet activation include high shear force, activation of the renin-angiotensin system, endothelial changes, and the presence of comorbidity, such as atrial fibrillation. The treatment of high blood pressure brings about a reversal of the changes seen in the cell. This could be in part due to the direct effect of the drug on the megakaryocyte and/or the platelets themselves, or it might simply be due to the reduction in blood pressure. Some drugs, such as calcium channel antagonists and angiotensin II receptor blockers, however, might have direct effects on platelet biochemistry other than reducing blood pressure. Finally, antiplatelet drugs are becoming an important part of the management of high-risk hypertensives, which aim to minimize vascular complications. (Hypertension. 2003;42:1-7.)

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Section: Calcium Channel Blockersmentioning

confidence: 99%

Pharmacological Modulation of Platelet Function in Hypertension

2003

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“…10 - 16 This elevation in platelet [Ca 2+ ]i in essential hypertension may reflect intracellular calcium levels in other tissues, including vascular smooth muscle, where increased vascular smooth muscle reactivity would be expressed as increased vascular resistance and elevated blood pressure. 17 The mechanism by which platelet [Ca 2+ ], is elevated in essential hypertension is yet to be identified.…”

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confidence: 99%

Calcitropic hormones, platelet calcium, and blood pressure in essential hypertension.

et al. 1990

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Plasma ionized calcium, platelet cytosolic calcium (using the fura-2 method in gel-filtered platelets), parathyroid hormone (both the intact hormone and a midmolecule portion), calcitriol, and calcidiol were measured in 19 untreated male patients with essential hypertension and 19 age-matched normotensive male research subjects. Mean levels of platelet cytosolic calcium, parathyroid hormone, calcitriol, and calcidiol were all significantly higher, whereas plasma ionized calcium was significantly lower, in the hypertensive group compared with the normotensive group. Both platelet cytosolic calcium and intact parathryoid hormone were positively correlated with mean arterial pressure (r=0.58, /?<0.001; r=0.S4, p<0.001, respectively), whereas plasma ionized calcium was inversely correlated with mean arterial pressure (r=-0.60, p<0.001) in the combined group of all study subjects. All three of these correlations were significant in the hypertensive group alone but not in the normotensive group alone. When analyzed with plasma ionized calcium, body mass index, serum calcitriol, and calcidiol in a multivariable regression model, the significance of the partial regressions of platelet cytosolic calcium and parathyroid hormone with mean arterial pressure persisted. Intact parathryoid hormone was positively correlated to platelet cytosolic calcium (r=0.43, p<0.01) and plasma ionized calcium was inversely correlated to platelet cytosolic calcium (r= -0.44,p<0.01). These results confirm previous reports of disturbances of calcium metabolism in essential hypertension and suggest that the elevated platelet cytosolic calcium observed in essential hypertension may be linked to one or more of these alterations of calcium metabolism. {Hypertension 1990;16:515-522) S everal studies have described disturbances of calcium metabolism in subjects with essential hypertension. McCarron 1 reported decreased plasma ionized calcium in patients with essential hypertension and also suggested that subjects with essential hypertension include less calcium in their diet.2 Further, McCarron and Morris 3 also found that supplementing the dietary calcium intake of subjects with essential hypertension could decrease the blood pressure of some subjects. The blood pressure-lowering effect of dietary calcium has also been observed in rat models of hypertension.

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“…Because of the relative availability of platelets and similarity of calcium-dependent contractile processes shared by platelets and vascular smooth muscle cells, 3 platelets have been used for analysis of the intracellular calcium metabolism. 4 Since the introduction of calcium-sensitive fluorescent dyes such as quin 2, fura-2, and indo-1 to measure [Ca 2+ ]j, 5 there have been several reports on the resting level of [Ca 2+ ]j in platelets from patients with essential hypertension 6 -8 and from spontaneously hypertensive rats (SHR) 9 -14 in comparison with their controls. For SHR, there is disagreement as to whether platelet [Ca 2+ ]i is increased.…”

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confidence: 99%