The effect of angiotensin II on the platelet aggregation induced by adenosine-diphosphate, epinephrine and thrombin

A, Poplawski

doi:10.1007/bf01900409

Cited by 23 publications

(9 citation statements)

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“…A vicious cy cle could thus result, with enhanced sensitiv ity to All allowing a progressive rise in sys temic blood pressure without compensatory uteroplacental vasodilatation. The increased platelet aggregability could follow from the altered PGI2/TXA2 ratio, with possibly a con tribution from All itself, which potentiates the pro-aggregatory effect of thrombin and adrenaline [24], The renal changes are also consistent with an enhanced intrarenal effect of All at the glomerulus. Furthermore, All has been shown to induce proteinuria in non-pregnant animals [25], possibly via an effect on vascular permeability.…”

Section: Lasupporting

confidence: 54%

Hypertension in Pregnancy: A Physiological Response to a Pathological Problem?

F¹

1989

Dev Pharmacol Ther

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In pregnancy-induced hypertension the secondary wave of trophoblast invasion fails, there is a progressive increase in pressor responsiveness to angiotensin II and an imbalance develops in the prostacyclin:thromboxane ratio towards thromboxane. As pregnancy progresses one can imagine that fetal demands gradually outstrip the ability of the relatively narrowed spiral arteries to perfuse the placenta. By analogy with renal artery stenosis, a defence mechanism would be stimulated (synthesis both of renin and vasodilator prostanoids) with systemic hypertension but improved perfusion. Where vasodilator synthesis is impaired, hypertension alone, with worsening perfusion, would ensue.

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Section: Lasupporting

confidence: 54%

Hypertension in Pregnancy: A Physiological Response to a Pathological Problem?

F¹

1989

Dev Pharmacol Ther

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“…Recent studies have shown that AngII has also non-hemodynamic effects, such as prothrombotic activity. Several studies suggest that AngII influences fibrinolysis [5]–[8], coagulation [9], [10] and platelet activation [11]–[14], which can promote thrombosis. Moreover, Mogielnicki et al found that AngII may enhance venous thrombus formation in vivo [15].…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II Upregulates Endothelial Lipase Expression via the NF-Kappa B and MAPK Signaling Pathways

Zhang¹,

Jiang

et al. 2014

PLoS ONE

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BackgroundAngiotensin II (AngII) participates in endothelial damage and inflammation, and accelerates atherosclerosis. Endothelial lipase (EL) is involved in the metabolism and clearance of high density lipoproteins (HDL), the serum levels of which correlate negatively with the onset of cardiovascular diseases including atherosclerosis. However, the relationship between AngII and EL is not yet fully understood. In this study, we investigated the effects of AngII on the expression of EL and the signaling pathways that mediate its effects in human umbilical vein endothelial cells (HUVECs).Methods and FindingsHUVECs were cultured in vitro with different treatments as follows: 1) The control group without any treatment; 2) AngII treatment for 0 h, 4 h, 8 h, 12 h and 24 h; 3) NF-κB activation inhibitor pyrrolidine dithiocarbamate (PDTC) pretreatment for 1 h before AngII treatment; and 4) mitogen-activated protein kinase (MAPK) p38 inhibitor (SB203580) pretreatment for 1 h before AngII treatment. EL levels in each group were detected by immunocytochemical staining and western blotting. HUVECs proliferation was detected by MTT and proliferating cell nuclear antigen (PCNA) immunofluorescence staining. NF-kappa B (NF-κB) p65, MAPK p38, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and phosphorylated extracellular signal-regulated kinase (p-ERK) expression levels were assayed by western blotting. The results showed that the protein levels of EL, NF-κB p65, MAPK p38, JNK, and p-ERK protein levels, in addition to the proliferation of HUVECs, were increased by AngII. Both the NF-kB inhibitor (PDTC) and the MAPK p38 inhibitor (SB203580) partially inhibited the effects of AngII on EL expression.ConclusionAngII may upregulate EL protein expression via the NF-κB and MAPK signaling pathways.

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“…The mechanisms of these changes in aggregation are not known, but human platelets have receptors for angiotensin II [6], and although angiotensin II does not cause aggregation itself, nanomolar or picomolar concentrations of angiotensin II in vitro potentiate the platelet aggregatory responses to adrenaline or adenosine diphosphate (ADP) [7,8], whereas higher concentrations (e. g. 10 7 mol. 1-1) inhibit adrenaline-induced aggregation [7].…”

mentioning

confidence: 99%

The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

Gow

Dockrell

Edwards

et al. 1992

Eur J Clin Pharmacol

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We have investigated the effect of varying sodium intake on the renin-angiotensin system, ADP-induced platelet aggregation in vitro, and blood 5-HT concentrations in 9 male volunteers. Systolic blood pressure was slightly reduced during a low sodium diet, whereas the diastolic pressure remained unchanged. Plasma renin activity and aldosterone concentration both fell significantly when sodium intake was increased; plasma angiotensin II concentration also fell, but not significantly. There was a significant fall in haematocrit after an increased sodium intake, but there was no change in the whole-blood platelet count after correcting for this. There were no significant changes in either total (i.e. PRP) or platelet 5-HT concentrations. The extent of platelet aggregation induced by 5 and 20 mumol.l-1 of ADP increased significantly when dietary sodium intake was increased. When compared with low or normal sodium intakes, lower concentrations of ADP were required to produce 50% of maximum aggregation after a high sodium intake. The 5-HT2 receptor antagonist ketanserin (1 mumol.l-1 in vitro) reduced the extent of aggregation induced by 5 mumol.l-1 ADP after the volunteers had taken a high sodium diet, whereas the angiotensin II receptor antagonist saralasin (1 nmol.l-1) increased the rate of aggregation after the low sodium diet. Thus, during a high sodium intake, human platelets become more sensitive to the aggregating agent ADP. It is possible that this effect is mediated via platelet 5-HT2 receptors, since ketanserin abolished the increase in salt-induced aggregation seen with 5 mumol.l-1 ADP.

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The effect of angiotensin II on the platelet aggregation induced by adenosine-diphosphate, epinephrine and thrombin

Cited by 23 publications

References 0 publications

Hypertension in Pregnancy: A Physiological Response to a Pathological Problem?

Hypertension in Pregnancy: A Physiological Response to a Pathological Problem?

Angiotensin II Upregulates Endothelial Lipase Expression via the NF-Kappa B and MAPK Signaling Pathways

The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

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