A total of 252 study subjects (126 Hypertensive and 126 healthy controls) were involved in this study to compare some hematological parameters among hypertensive and normotensive individuals. The mean age of hypertensive and control individuals were 50.3 ± 11 and 49.8 ± 11.6 years, respectively. Based on the result, hypertensive groups had significantly higher median (IQR) WBC value 6.9 × 103/μl (3.7 × 103/μl) when compared to apparently healthy normotensive controls 5.2 × 103/μl (2.2 × 103/μl). This finding is in agreement with other similar studies by Babu KR et al.  and Al-Muhana et al. . Also, this study showed a significant positive correlation of WBC count with diastolic blood pressure, systolic blood pressure and mean arterial pressure.
There is a causal relationship between vascular function and different hematological disorders [17, 20]. Most hypertensive patient’s exhibit increased blood viscosity compared with healthy controls . There is a decreased RBC deformability which could cause an increased microvascular flow resistance, which may result in haemolysis and organ damage . This haemolysis induces release of Hgb in to the plasma which scavenges nitric oxide and causes endothelial dysfunction . There is also functional alterations and abnormalities of platelets in hypertension which is associated with increased risk of clot formation. Activated and large platelets are produced as a result of endothelial dysfunction. These large and activated platelets produce vasoconstrictors. This enhances narrowing of blood vessels; there by high blood pressure and thrombotic disease [22,23,24,25].
The relationship between WBC and hypertension may be explained by an increased concentration of stem cell factor (SCF) in serum . During HTN, there is a vascular endothelial dysfunction [27, 28]. Thus, to repair this dysfunction SCF/c-kit increases. The SCF has an important role in differentiation and proliferation of haematopoietic cells [26, 29]. This pathway might increase WBC via its participation in the differentiation and proliferation of haematopoietic cells. Additionally, white blood cells are inflammatory marker and tends to increase during HTN which is supported by Kim D-J et al. . But in contradiction to this study, a study conducted in São Paulo, Brazil showed lower mean value of WBC count in hypertensive individuals when compared to apparently healthy normotensive subjects. But there was no significant association . This difference may be due to differences in the study subjects. The study subjects included in this study were HTN confirmed but the study subjects in São Paulo, Brazil were without a previous diagnosis of high blood pressure.
Similarly, the current study showed significantly higher median (IQR) RBC value 5 × 106/μl (0.88 × 106/μl) when compared to apparently healthy controls 4.88 × 106/μl (0.58 × 106/μl). This is supported by Babu KR et al. , Reis RS et al.  and Bruschi G et al. . Also, RBC count showed significantly positive correlation with diastolic blood pressure, systolic blood pressure and mean arterial pressure. The possible mechanisms of the association between RBC and blood pressure are not entirely known but the study showed that it may be associated with stem cell factor. Stem cell factor (SCF)/c-kit signaling proteins are increased in hypertensive individuals . Since it is involved in repairing of damaged blood vessels, the expression of stem cell factor (SCF)/c-kit signaling proteins are relatively high during blood vessel repair. Thus, as a result of SCF, RBC number will be increase via the participation of SCF in the differentiation and proliferation of haematopoietic cells .
In the present study, Hgb value was significantly increased in the hypertensive group compared to normotensive groups. This findings is in agreement with supported studies done by Babu KR et al.  and Al-Muhana et al. [2, 19] but it contradicts with a study conducted in São Paulo, Brazil . Hgb value has shown a positive correlation with systolic, diastolic and mean arterial pressure in hypertensive groups which is similar to the study conducted by Atsma F et al. in France .
The association between HTN and Hgb level may be explained by Hgb and arginase enzyme effects on nitric oxide (NO) bioavailability [21, 34]. During HTN, there is a possibility of hemolysis. But, whether hemolysis is a cause or effect of hypertension remains unclear. Most studies suggest that hypertension is a complication of hemolysis and associated with hemolytic anemia . In addition to this, blood disorders such as polycythemia vera and essential thrombocythemia, causes hypertension . Polycythemia vera will cause an increase in relative red cell mass and whole blood viscosity, and thereby increase peripheral resistance to blood flow. If there is peripheral resistance in the microcirculation, there will be a possibility of hemolysis . During hemolysis, hemoglobin and arginase enzyme are released in to circulation from erythrocytes. This free Hgb is scavenger of nitric oxide which is produced in the endothelial cell that lines the blood vessels and important for relaxation of blood vessels. On the other hand, arginase enzyme depletes the substrate used for NO synthesis by conversion of arginine to ornithine, thus reducing NO production. This conditions leading to endothelial dysfunction and ultimately activation of platelets and clots [21, 36, 37]. Therefore, if free Hgb scavenges nitric oxide and arginase enzyme depletes substrates used for NO production, blood vessel dilation decreases, which in turn causes increased blood pressure.
In our study, the median (IQR) value of HCT significantly increased in hypertensive individuals compare to normotensive individuals. These findings are also familiar to Babu KR et al. . In bivariate correlation analysis, HCT value has shown a positive correlation with systolic, diastolic and MAP blood pressure in hypertensive groups. The reasonable mechanisms underlying the association between HCT and blood pressure is that HCT is a determinant factor for high whole blood viscosity during hypertension. This may lead to a peripheral resistance to blood flow and high blood pressure [7, 11]. The evidence showed that, most hypertensive patients exhibit increased blood viscosity compared with healthy controls . Therefore, high hematocrit in hypertension could reflect a true increase in red blood cell mass as well as hemo-concentration caused by a reduction in plasma volume. In contrary to aforementioned result, contradicted study conducted at University of Port Harcourt teaching hospital, Nigeria  and Saudi Arabia  reported that HCT was not significantly differ between hypertensive patients and normotensive individuals. This difference may be due to difference in sample size.
In our study, RDW increased significantly in hypertensive groups compared to normotensive individuals. Most studies suggest that higher RDW, which is a measure of the variability in the circulating erythrocytes’ size, may be resulted from ineffective erythropoiesis due to chronic inflammation during hypertension [39, 40].
In this study MCV and MCHC were increased significantly in hypertensive groups but there were no significant differences in MCH. But other studies in these parameters showed contradicted ideas. For example a study conducted by Babu KR et al.  showed significantly lower MCV, significantly higher MCHC and higher but no difference MCH value. In São Paulo, Brazil, MCV were similar , in France MCV is lower by 2%  and a study in Saudi Arabia showed no significant differences of MCV, MCH and MCHC .
In the present study, the median (IQR) value of PLT count, mean value of MPV and PDW were increased in hypertensive groups than controls. Even though statistically not significant, median value of PLT count was slightly higher in hypertensive groups. The possible explanation for this could be related to consumption of platelets. During hypertension, there is endothelial dysfunction and this leads to platelet activation and clot formation. Then platelets will be consumed and there number does not increase as expected [25, 41, 42]. However, statistically significant increment of MPV and PDW were found in hypertensive groups compared to normotensive groups. This finding is in accordance with the previous findings by Babu et al. , Al-Muhana et al. , Bruschi et al.  and Ates et al. .
In our study, PLT count positively correlated with blood pressure indices. The possible mechanisms might be related to vascular complication in hypertensive groups. High blood pressure causes endothelial damage via shear stress, which results in an increase in platelet activation . When platelet production is induced, there could be increment in platelet count, MPV and PDW . Evidence suggests that PLT consumption increase at the site of injured blood vessel. During this condition larger PLTs would be released from the bone marrow because larger PLTs are hemostatically more active than mature PLT. Because larger PLTs are hemostatically more active, the presence of larger PLTs is probably a risk factor for developing coronary thrombosis and myocardial infraction [41, 42].
Since antihypertensive therapy reduces blood pressure and improve endothelial function, their effect didn’t assess in this study. Additionally, cell free hemoglobin analysis was not considered. Therefore, further cohort study is required.