Hypertension is an important public health problem affecting more than 50 million individuals in the USA alone. The most common form,
essential hypertension, results from the complex interplay between
genetic predisposition and environmental influences. Epidemiological, migration, intervention and genetic studies in humans and animals provide very strong evidence of a causal link between high
salt intake and
high blood pressure. One of the candidate genes for
salt-sensitive
hypertension is
adducin.
Adducin is a heterodimeric cytoskeleton
protein, the three subunits of which are encoded by genes (ADD1, ADD2 and ADD3) that map to three different chromosomes. A long series of parallel studies in the Milan hypertensive rat strain model of
hypertension and humans indicated that an altered
adducin function might cause
hypertension through enhanced constitutive tubular
sodium reabsorption. An example of a prospective efficacy of pharmacogenetics and pharmacogenomics is the detection and impact of
adducin polymorphisms on
hypertension. In particular, the selective advantages of
diuretics in preventing
myocardial infarction and
stroke over other
antihypertensive therapies that produce a similar blood pressure reduction in carriers of the mutated
adducin may support new strategies aimed at optimizing the use of new
antihypertensive agents for the prevention of
hypertension-associated organ damage.