One of the major pathophysiological features of
primary hypertension is an inappropriate activation of the
sympathetic nervous system, which is mediated by excessive synthesis and
secretion of
catecholamine into the
blood.
Tyrosine hydroxylase (TH), a rate-limiting
enzyme in the synthesis of
catecholamine, has been highlighted because
genetic variations of TH could alter the activity of the
sympathetic nervous system activity and subsequently contribute to the pathogenesis of
hypertension. Here, we discuss the
role of TH as a regulator of sympathetic activity and
review several studies that investigated the relationship between
genetic variations of TH and
hypertension.