Eprosartan is a potent, non-peptide, orally active
non-biphenyl non-tetrazole angiotensin II antagonist, which binds selectively to the AT1 receptor.
Angiotensin II is a potent vasoconstrictor and the
primary active hormone of the reninangiotensinaldosterone system, playing a major part in the
pathophysiology of hypertension.
In addition, in animals eprosartan was shown to
block the direct vasoconstrictor response to angiotensin as well as the indirect effects mediated by
enhanced neurotransmission, indicating the potential to antagonize overactivity of the sympathetic
nervous system.
Eprosartan antagonised the effect of angiotensin
II on blood pressure, renal blood flow and
aldosterone secretion in normal volunteers. Blood
pressure control is maintained over a 24 hour
period with no first dose postural hypo tension or reflex tachycardia. Discontinuation of treatment
with eprosartan does not lead to a rapid rebound
increase in blood pressure.
Eprosartan does not compromise renal autoregulatory mechanisms. In normal adult males eprosartan
has been shown to increase mean effective renal
plasma flow. Eprosartan maintains renal function in
patients with essential hyper tension and patients
with renal insufficiency.
Eprosartan does not potentiate effects relating to
bradykinin (mediated by ACE inhibition) e.g. cough.