Genetics & Hypertension (Commentary) (Report‪)‬

Hypertension is a complex disease involving interaction of many risk genes and environmental factors such as obesity, dietary salt intake, alcohol consumption, and stress. Approximately 20 to 60 per cent of the population variability in blood pressure is genetically determined (1). In the last decade, a large number of candidate genes have been tested for association with blood pressure and hypertension without convincing results. Polymorphisms in genes of renin-angiotensin-aldosterone system (RAAS) comprising of angiotensinogen (AG7), angiotensin-converting enzyme (ACE), angiotensin II receptor type 1 (AT1R), and aldosterone synthase (CYP11B2) genes have been the most commonly studied for association with various aspects of hypertension. No single gene within the RAAS appears to predominate in the association studies and there appears to be an increasing complexity and sophistication in association studies involving RAAS. Haplotypes involving several polymorphisms in a single gene have been found to be better predictors than a single nucleotide polymorphism (SNP) (2). Further, adding to complexity are the observations that these genetic associations may vary according to hypertensive phenotypes (systolic, diastolic or pulse-components), with age and gender as confounding elements (3). For example, ACE gene polymorphism was specifically found to be associated with reduced diastolic blood pressure in men who were older than 50 years (4).