In addition to hypercholesterolaemia and smoking, hypertension, a chronic disease with many cardiovascular complications, is one of the major risk factors for cardiac ischaemia, and the main risk factor for cerebrovascular diseases. Recent studies indicate that in hypertensive patients, there is an elevated free radical generation and increased lipid peroxidation and derived oxidized products; also there is imbalance in antioxidant status. Although some of the functions of magnesium, copper, and zinc have been known for sometimes, recent studies have shown that these elements are involved in the pathogenesis of certain cardiovascular diseases particularly hypertension. Studies also demonstrate that some antihypertensive drugs may cause some unwanted effects on lipid profile and trace elements metabolism. The present study includes measurement of lipid peroxide profile, lipid profile, some trace elements, and minary protein in 69 patients aged 30-70 years (mean age = 50.52 + 8.71 years). They were classified into three main groups according to the type of therapy: 1. Hypertensives on Atenolol therapy (n=27, age range = 34-70 years). 2. Hypertensives on Captopril therapy (n=27, age range = 30-65 yearsO. 3. Hypertensives on no pharmacological antihypertensive therapy (NPAHT) (n = 15, age range = 32-64 years). The results were compared with 45 apparently healthy controls (age range = 30-66 years). The results showed significant elevation in serum malondialdehyde (MDA) and percentage of oxidized non high-density lipoprotein (OX.non-HDL %) and significant reduction in percentage of oxidized high-density lipoprotein (OX.HDL %) as compared to the controls. The disturbance in the oxidant / antioxidant balance happened despite the treatment and blood pressure control. This could be attributed to the presence of hypertension as a causative factor or the presence of undesirable side effects of the drug. Different types of treatment gives variable pictures of lipid peroxides, the best picture was seen in the group of hypertensives on captopril; this was supported by the significant difference between different hypertensive groups as compared with each other. Hyperlipidaemia in hypertensives involved an increase in serum triglyceride (TG) and serum total cholesterol (TC) with a decrease in serum high-density lipoprotein cholesterol (HDL-C) in hypertensives on Atenolol therapy. All patient's groups had the risk of developing atherosclerosis particularly those on NPAHT according to the TG: HDL-C ratio (LDL size index), which reflects the presence of small, dense low-density lipoprotein (LDL) particles. There was no significant difference in serum magnesium in hypertensives as compared to controls and as compared with each other, indicating that extra cellular magnesium, apparently, has no role in the pathogenesis of hypertension. Serum copper was significantly increased in hypertensives on NPAHT but no significant difference was seen when PAHT was used. In contrary, serum zinc was significantly reduced in hypertensives on PAHT and it was not altered in those not receiving medications; however, zinc: copper ratio was significantly reduced in hypertensive on different treatment modalities; indicating the influence of hypertension and antihypertensive drugs on zinc / copper status. In conclusion, hypertensives on different modalities of therapy experienced oxidative stress, hyperlipidaemia, altered zinc / copper status, but normal serum magnesium levels. The suggested mechanisms underlying these events are discussed.