Eprosartan may have a unique mechanism of action in lowering systolic blood pressure by inhibiting pre-synaptic AT1 receptors and reducing sympathetic nervous system activity.
The sympathetic nervous system is intimately involved in both the origin and the perpetuation of the hypertensive state, although there is some debate as to its precise contribution to the long-term hypertensive condition. Catecholamines are leading candidates to be both the pressor mechanism that initiates the rise in blood pressure and the trophic mechanism that maintains hypertension by vascular hypertrophy. Although the relationship between sympathetic nervous system and systolic blood pressure would seem intuitive, the multiple interactive pathways between these two pathways still needs to be more completely clarified, particularly as relates to interplay with the renin-angiotensin axis. Along this line of reasoning, a number of studies have examined the interplay between ACE inhibitors or angiotensin-receptor antagonists and alterations in sympathetic nervous system activity. Recent data support a role for one of the angiotensin-receptor antagonists, eprosartan, in having a potent inhibitory effect on pre-synaptic type-1 angiotensin receptors (AT(1) -receptors) involved in the enhancement of sympathetic nervous system activity. This may provide an explanation for the differential effect on systolic blood pressure exhibited by this compound.
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Domenic A. Sica (2000) studied this question.
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