Hypertension (HTN) is also called high blood pressure. It is a condition in which systemic arterial pressure is elevated above the threshold value [1]. It is expressed by systolic (maximum) and diastolic (minimum) arterial pressures. Systolic pressure is occurring during contraction of the left ventricle of the heart while diastolic pressure is occurring before the next contraction. Normally at rest the systolic pressure is within 100–140 mm mercury (mmHg) and diastolic pressure is within 60–90 mmHg [2, 3]. Based on the seventh Joint National Committee (7 JNC) report in 2008, normal HTN was defined as systolic blood pressure (SBP) < 120 mmHg and diastolic blood pressure (DBP) < 80 mmHg, pre-HTN with SBP of 120-139 mmHg or DBP 80–89 mmHg, stage I HTN with SBP of 140–159 mmHg or DBP 90–99 mmHg and stage II HTN with SBP ≥ 160 mmHg or DBP ≥ 100 mmHg [1, 4].

HTN can be categorized in to two; primary and secondary hypertensions. Primary HTN, which consists of about 95% cases, can occur without any obvious underlying causes while secondary HTN is developed due to secondary to diseases such as kidney disease, endocrine disorders and narrowing of the aorta or kidney arteries [5, 6].

HTN is a major health problem worldwide that affects 20–30% of the adult population [7]. It is rapidly increased from 3% in rural areas to 30% in urban areas of Sub-Saharan Africa. In 2008, its overall prevalence rate in Sub Saharan Africa was 16.2% ranging from 10.6% (Ethiopia) to 26.9% (Ghana) [8–10].

HTN may lead to severe end-organ damage, coronary heart disease and stroke which constitute the leading cause of mortality [11, 12]. It is strongly associated with functional and structural abnormalities to organs that involve in hematopoiesis [5, 6, 13] and blood viscosity is increased in most hypertensive patient’s [14]. Although, the details of this association is unclear, development of HTN is accompanied by reduction in deformability, and an increase in size, number and aggregability of red blood cells. These abnormalities of the red cells may worsen the microcirculation and enhance an end-organ damage [11, 15].

On the other hand, HTN has an impact on hematological parameter such as hematocrit (HCT), hemoglobin (Hgb), red blood cell (RBC) count, white blood cell (WBC) count and platelet (PLT) count. Impaired hematological parameters may strongly indicate hypertensive end-organ damage, specifically kidney failure [7, 16, 17]. Specifically increased Hgb level may cause left ventricular hypertrophy while low Hgb levels causes anemia and heart failure [18].

Generally, there are contradictory results regarding hematological parameters of hypertensive patients in different countries. Moreover, there is lack of information regarding to hematological parameters in hypertensive patients in Ethiopia. Therefore, this study was aimed at assessing hematological parameters in hypertensive patients in comparison with apparently healthy individuals and correlating hematological parameters with blood pressure indices (systolic blood pressure, diastolic blood pressure and mean arterial pressure) at university of Gondar hospital, Northwest Ethiopia.

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. [7] and Al-Muhana et al. [19]. 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 [14]. There is a decreased RBC deformability which could cause an increased microvascular flow resistance, which may result in haemolysis and organ damage [11]. This haemolysis induces release of Hgb in to the plasma which scavenges nitric oxide and causes endothelial dysfunction [21]. 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 [22–25].

The relationship between WBC and hypertension may be explained by an increased concentration of stem cell factor (SCF) in serum [26]. 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. [30]. 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 [31]. 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. [7], Reis RS et al. [31] and Bruschi G et al. [32]. 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 [26]. 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 [29].

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. [7] and Al-Muhana et al. [2, 19] but it contradicts with a study conducted in São Paulo, Brazil [31]. 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 [33].

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 [35]. In addition to this, blood disorders such as polycythemia vera and essential thrombocythemia, causes hypertension [20]. 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 [21]. 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. [7]. 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 [14]. 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 [38] and Saudi Arabia [19] 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. [7] showed significantly lower MCV, significantly higher MCHC and higher but no difference MCH value. In São Paulo, Brazil, MCV were similar [31], in France MCV is lower by 2% [32] and a study in Saudi Arabia showed no significant differences of MCV, MCH and MCHC [19].

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. [7], Al-Muhana et al. [19], Bruschi et al. [32] and Ates et al. [43].

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 [43]. When platelet production is induced, there could be increment in platelet count, MPV and PDW [44]. 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.

In the present study, the median (IQR) value of WBC, RBC, Hgb, HCT, MCV and the mean value of MCHC, RDW, MPV and PDW were significantly higher in the hypertensive group compared to apparently healthy controls. But platelet count and MCH showed no statistically significant difference between hypertensive and normotensive groups. In this study there was statistically significant positive correlations of WBC, RBC, Hgb, HCT and PLT with blood pressure indices (diastolic blood pressure, systolic blood pressure and mean arterial pressure) among hypertensive individuals. Impaired hematological parameters may strongly indicate hypertensive end-organ damage. Hematological complication such as RBCs reduction in deformability and an increase in the size causes hemolysis, high Hgb and low levels are associated with cardiovascular risk and activation of platelets is risk factor for thrombotic diseases observed during hypertension. Therefore, it is important to assess changes in hematological parameters for hypertensive patients which may help to prevent such complications associated hematological disorders.