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Purpose: Preeclampsia is a multisystem disorder and its etiology remains still unclear. Recent hypotheses rely on imbalance between angiogenic and antiangiogenic factors and disruption of endothelial function of spiral arteries. In addition; increased VTE (venous thromboembolism) risk is still unclear in preeclampsia. Our aim was to investigate the relationship between endothelial dysfunction, adipocytokines, platelet function, and vasculogenesis in preeclampsia., Methods: Plasma angiogenic (PlGF, VEGF), antiangiogenic factors (sflt-1, endoglin) with adipocytokines (leptin, adiponectin, ghrelin), endothelial dysfunction markers (vWF, NO), and platelet function markers (ADP and collagen induced platelet aggregation, P-selectin) were examined in 30 early-onset, 22 late-onset preeclampsia, and 27 healthy pregnants. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum biomarker levels except NO. NO levels were determined using colorimetric method., Results: Endoglin, leptin, and vWF levels were increased in preeclampsia (P < 0.001), whereas PlGF, P-selectin (P < 0.001), and col-induced platelet aggregation slope (P < 0.05) were decreased in the same counterpart as compared to healthy pregnants. Endoglin also correlated with sflt-1 in preeclamptic patients., Conclusion: Increase in the levels of antiangiogenic factors and leptin herewith decline in the level of other angiogenic factor PlGF, did not affect nitric oxide and platelet aggregation markers significantly. Increased levels of vWF and endoglin might be result of endothelial dysfunction, so our findings suggest that an impaired angiogenesis may address endothelial dysfunction, but not platelet aggregation for preeclampsia.

The aim of the present study is to determine and correlate adiponectin, homocysteine, nitric oxide, and ADP-induced platelet aggregation levels in untreated patients with essential hypertension and healthy individuals. A total of 36 individuals, 23 untreated patients with essential hypertension and 13 healthy individuals, were included in the scope of this study. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum adiponectin and TNF-alpha levels. The levels of serum homocysteine were measured by using competitive chemiluminescent enzyme immunoassay. Serum concentrations of hsCRP were measured by the Nephelometer. Plasma nitrite, nitrate, and total nitric oxide (NOx) levels were determined by colorimetric method. Homocysteine and hsCRP levels in patients with essential hypertension were found to be significantly higher than those in the control group (P = 0.02, P = 0.001, respectively). The average platelet aggregation levels in patient group were higher than control group, but there were no statistically significant differences between them (P > 0.05). In addition, in patients with essential hypertension adiponectin and nitrite levels are significantly lower than control group (P < 0.001, P = 0.045, respectively). We have also found significant correlations between nitrite-platelet aggregation amplitude, nitrite-platelet aggregation slope, nitrite-adiponectin, homocysteine-platelet aggregation amplitude, and sistolic blood pressure-platelet aggregation amplitude levels (r = -0.844; P < 0.001, r = -0.680; P = 0.011, r = 0.454; P = 0.05, r = 0.414; P = 0.05, r = 0.442; P = 0.035, respectively). Increased homocysteine and decreased adiponectin serum levels in patients with essential hypertension correlate well with changes in ADP-induced conventional platelet aggregation. This association may potentially contribute to future thrombus formation and higher risks for cardiovascular events in hypertensive patients.

Several studies indicate that thrombosis plays an important role in the pathogenesis of coronary heart disease (CHD). Fibronectin is a multifunctional protein in plasma, other body fluids, and cell surface and plays an important role in platelet functions, including mediation of cell-cell and cell-surface interactions. Sialic acid is a regular constituent of glycoproteins and gangliozides in the outer cell membrane of mammalian cells. Therefore, the sialic acid content of platelets, which are characterized by their ability to aggregate with each other, can be important in leading to thrombus formation. In this study, platelet fibronectin, sialic acid-, and adenosine diphosphate (ADP)-induced platelet aggregation levels were determined in patients with CHD. Platelet sialic acid concentrations were determined by Warren's method. Platelet aggregation tests with ADP in platelet-rich plasma (PRP) were analyzed by use of an aggregometer. Platelet homogenate fibronectin levels were determined by ELISA. Total protein levels were determined by Lowry method. Our results indicate that, in patients with no vessel disease (patients with no obstructed vessel but suffering from chest pain, like angina pectoris) platelet fibronectin levels were significantly lower than the total of the other patients (patients with 1, 2, or 3 obstructed coronary vessels) (p<0.05). Sialic acid levels in patients with no vessel disease were significantly lower than the total of the patient group (p<0.05). There was significant (+) correlation between platelet aggregation, platelet fibronectin, platelet sialic acid, and severity of disease (p<0.05). Our preliminary findings suggest that, especially platelet fibronectin levels potentially represent a pathogenic factor for CHD.

Introduction: Coronary thrombosis is an important determinant of prognosis in patients with acute coronary syndromes. Fibronectin is also found in platelets within the alpha secretory granules and secreted following platelet stimulation by a variety of agonist. Available data suggest that expression of platelet fibronectin on the cell surface may indicate a role in platelet aggregation and adhesion to fibrin thrombi and connective tissue. Clear evidence has emerged that a concerted action of nitric oxide (NO) generated by either endothelial or platelet NO synthases regulates platelet activation, causing inhibition of adhesion and aggregation. The aim of the present study was determining and correlating the serum total NO (NOx), platelet fibronectin and ADP-induced platelet aggregation levels in coronary artery disease (CAD) patient subgroups., Materials and Methods: A total of 43 coronary artery disease patients were included in this study. Peripheral blood samples from patients with coronary artery disease were obtained from the Department of Cardiology. Platelet aggregation tests with adenosine diphosphate (ADP) were analyzed by using aggregometer. Platelet fibronectin concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Serum total nitric oxide (NOx) levels were determined by colorimetric method., Results: In patients with double-vessel disease, platelet fibronectin levels were found to be significantly higher than no-vessel disease (p<0.001), single-vessel disease (p<0.01) and triple-vessel disease (p<0.001). In addition, in patients with single-vessel disease platelet fibronectin levels significantly higher than no-vessel disease (p<0.05). We could not find any significant differences in ADP-induced platelet aggregation and serum NOx values between CAD patient subgroups. There was a positive correlation between platelet fibronectin levels and severity of disease (r=0.315, p<0.05).

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 +/- 12.8 and 149.2 +/- 17.3 mmHg, respectively. Mean DBP decreased from 93.7 +/- 8.2 to 87.7 +/- 10.3 mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% +/- 24.3% before and 58.3% +/- 18.1% after the treatment. The same variables with ristocetin were 66.8% +/- 21.6% and 60.8% +/- 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.