Angiotensin II is the most vasoactive peptide and a powerful blood vessels constrictor of renin-angiotensin-aldosterone system (RAAS). It affects arterial musculature, increases peripheral resistance, and raises blood pressure (BP). The majority of angiotensin II's effects are mediated by the angiotensin II type 1 receptor (ATR1). To investigate the impact of A1166C single nucleotide polymorphism (SNP) of ATR1 gene on cardiovascular and renal complications in Iraqi hypertensive patients treated with candesartan. Ninety-two patients with essential hypertension taking 8 mg/day candesartan from not less than three months were recruited for the investigation from Imam Hussein Teaching Hospital and from private clinic in Karbala province, Iraq. Blood pressure, heart rate and echocardiography reports were recorded. The analysis of biochemical parameters such as serum creatinine, urea, angiotensinogen, angiotensin II and some electrolytes levels were done. The tetra-primer amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) was used for genotyping of the A1166C SNP. The distribution of A1166C SNP in the hypertensive patients was 54.35% AA, 40.22% AC and 5.43% CC. There was no association between A1166C and echocardiogram, biochemical or BP parameters (P>0.05) except heart rate; patients with AA genotype have higher heart rate (88.32±10.64, P=0.005) than patients with AC and CC genotype. The CC genotype of A1166C is the less frequent than other two genotypes of this SNP in Iraqi hypertensive patients. The A1166C SNP has neither an effect on hypertension complication nor on the patients’ response to candesartan in Iraqi hypertensive patients.