AT1-receptor blockade and sympathetic neurotransmission in cardiovascular disease

Authors: Nap, A.; Balt, J. C.; Mathy, M. J.; van Zwieten, P. A.

Source: Autonomic & Autacoid Pharmacology, Volume 23, Numbers 5-6, October 2003 , pp. 285-296(12)

Publisher: Blackwell Publishing

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Abstract:

Summary

1 The present survey is dealing with the interactions between the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system (SNS) in various organs and tissues, with an emphasis on the angiotensin AT-receptors located at the sympathetic nerve endings.

2 Angiotensin II, the main effector of the RAAS is known to stimulate sympathetic nerve traffic and its sequelae in numerous organs and tissues, such as the central nervous system, the adrenal medulla, the sympathetic ganglia and the sympathetic nerve endings. These stimulatory effects are mediated by AT1-receptors and counteracted by AT1-receptor antagonists.

3 Sympatho-inhibition at the level of the sympathetic nerve ending appears to be a class effect of the AT1-receptor blockers, mediated by presynaptic AT1-receptors. With respect to the ratio pre-/postsynaptic AT1-receptor antagonism important quantitative differences between the various compounds were found.

4 Both the pre- and postjunctional receptors at the sympathetic nerve endings belong to the AT1-receptor population. However, the presynaptic receptors belong to the AT1B-subtype, whereas the postjunctional receptors probably belong to a different AT1-receptor subpopulation.

5 Sympatho-inhibition is a class effect of the AT1-receptor antagonists. In conditions in which the SNS plays a pathophysiological role, such as hypertension and congestive heart failure, this property may well be of therapeutic relevance.

Keywords: angiotensin; sympathetic nervous system; presynaptic AT1-receptors; postsynaptic AT1-receptors; renin-angiotensin-aldosterone system; cardiovascular disease

Document Type: Research article

DOI: 10.1111/j.1474-8673.2004.00301.x

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