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Rupp H, Jäger B  
The renin-angiotensin system and the sympathetic nervous system in hypertension and congestive heart failure: implications for therapeutic interventions

Journal of Clinical and Basic Cardiology 2001; 4 (1): 47-51

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Fig. 1: RAS und SNS Fig. 2: Sympathisches Nervensystem - Blutgefäß Fig. 4: Angiotensin-II-Antagonisten - Strukturformel

Keywords: EprosartanRenin-Angiotensin-Systemsympathisches NervensystemEprosartanrenin-angiotensin systemsympathetic nervous system

The renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) are both contributors to the development and maintenance of hypertension. It has recently been recognised that extensive interactions occur between the RAS and SNS. In addition to the classical interactions occurring between the SNS and RAS on an organ and cellular level, there is evidence that disordered subcellular crosstalk can occur between the effectors of the SNS and angiotensin II. This results in the promotion of structural remodelling of cardiac tissue seen in both hypertension and congestive heart failure. Therefore, optimal drug therapy for hypertension and congestive heart failure would attenuate both the RAS and SNS while also restoring the balance of disordered crosstalk between the systems. AT1 receptor blockers are the most recent class of cardiovascular therapeutic agents. Preclinicial studies to date show that the antihypertensive effects of AT1 receptor blockers may be mediated through their effects on the SNS as well as the RAS. Eprosartan was found to be more potent in its effects on the sympathetic nervous system than other non-peptide AT1 receptor blockers and shows the lowest ratio between the effective doses on RAS and SNS. This high sympatholytic potency may be a result of differences in chemical structure and receptor-binding characteristics of eprosartan when compared with other AT1 receptor blockers. It remains to be seen whether these potentially significant therapeutic implications for hypertension and congestive heart failure translate into the clinical setting. J Clin Basic Cardiol 2001; 4: 47-51.
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