Impact of Renin–Angiotensin–Aldosterone System (RAAS) Gene Polymorphism in Essential Hypertension and Antihypertensive Drug Therapy: A Review

Figures

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  Figure 1. RAAS gene polymorphisms. Explanation for the figure: angiotensinogen (AGT) is cleaved by renin to angiotensin I (Ang I), which is further hydrolysed to angiotensin II (Ang II) by angiotensin converting enzyme (ACE). Ang II has two types of receptors: angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R). On one hand, Ang II then binds with AT1R, which directly acts on blood vessels and adrenal glands to increase blood pressure. During this process, aldosterone synthase helps in the secretion of aldosterone that facilitates the reabsorption of sodium and water, thereby increasing BP. On the other hand, AT2R is responsible for vasodilation. There are many gene polymorphisms seen in the RAAS system, such as AGT (M235T), ACE (insertion/deletion) (I/D), Ang II Type 1 receptor (AT1R) (A1166C) and aldosterone synthase (C344T).

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  Figure 2. Illustration of AT1R (A1166C) gene polymorphism representing a higher prevalence of risk of EH in the patient carrier of the C genotype.

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  Figure 3. Illustration of antihypertensive drug variance among whites and blacks.

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  Figure 4. Illustration of variation in drug response among different populations.