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Molecular interactions of vasoactive systems in cardiovascular damage.
J Cardiovasc Pharmacol. 2001 Nov; 38 Suppl 2:S7-9.JC

Abstract

The renin-angiotensin system (RAS) and the kallikrein-kinin system (KKS) are important in the aetiology of hypertension and the pathogenesis of cardiac and renal damage associated with elevated blood pressure. While angiotensin II acts by increasing blood pressure and supporting end-organ damage, kinins have an opposite protective effect. The two systems interact on many levels. Angiotensin-converting enzyme (ACE) activates angiotensins and inactivates kinins. ACE inhibitors therefore exert their organ-protective action via both systems, as they block the deleterious RAS and potentiate the protective KKS. Furthermore, ACE may directly interact with the kinin B2 receptor and ACE inhibitors, thereby eliciting a resensitization of this receptor following agonist-induced desensitization. Recently, a functional heterodimer of AT1 and B2 receptors has also been demonstrated. Moreover, kallikreins may be involved in the activation of prorenin and in the signalling pathway of angiotensin AT2 receptors. Because of the multitude of interactions, any therapeutic intervention into one of the two peptide systems will automatically lead to an alteration in the other. This double action is utilized by drugs such as ACE inhibitors to provide unprecedented effectiveness in hypertension and associated cardiac and renal damage.

Authors+Show Affiliations

Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany. mbader@mdc-berlin.de

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11811382

Citation

Bader, M. "Molecular Interactions of Vasoactive Systems in Cardiovascular Damage." Journal of Cardiovascular Pharmacology, vol. 38 Suppl 2, 2001, pp. S7-9.
Bader M. Molecular interactions of vasoactive systems in cardiovascular damage. J Cardiovasc Pharmacol. 2001;38 Suppl 2:S7-9.
Bader, M. (2001). Molecular interactions of vasoactive systems in cardiovascular damage. Journal of Cardiovascular Pharmacology, 38 Suppl 2, S7-9.
Bader M. Molecular Interactions of Vasoactive Systems in Cardiovascular Damage. J Cardiovasc Pharmacol. 2001;38 Suppl 2:S7-9. PubMed PMID: 11811382.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Molecular interactions of vasoactive systems in cardiovascular damage. A1 - Bader,M, PY - 2002/1/29/pubmed PY - 2002/7/23/medline PY - 2002/1/29/entrez SP - S7 EP - 9 JF - Journal of cardiovascular pharmacology JO - J. Cardiovasc. Pharmacol. VL - 38 Suppl 2 N2 - The renin-angiotensin system (RAS) and the kallikrein-kinin system (KKS) are important in the aetiology of hypertension and the pathogenesis of cardiac and renal damage associated with elevated blood pressure. While angiotensin II acts by increasing blood pressure and supporting end-organ damage, kinins have an opposite protective effect. The two systems interact on many levels. Angiotensin-converting enzyme (ACE) activates angiotensins and inactivates kinins. ACE inhibitors therefore exert their organ-protective action via both systems, as they block the deleterious RAS and potentiate the protective KKS. Furthermore, ACE may directly interact with the kinin B2 receptor and ACE inhibitors, thereby eliciting a resensitization of this receptor following agonist-induced desensitization. Recently, a functional heterodimer of AT1 and B2 receptors has also been demonstrated. Moreover, kallikreins may be involved in the activation of prorenin and in the signalling pathway of angiotensin AT2 receptors. Because of the multitude of interactions, any therapeutic intervention into one of the two peptide systems will automatically lead to an alteration in the other. This double action is utilized by drugs such as ACE inhibitors to provide unprecedented effectiveness in hypertension and associated cardiac and renal damage. SN - 0160-2446 UR - https://www.unboundmedicine.com/medline/citation/11811382/Molecular_interactions_of_vasoactive_systems_in_cardiovascular_damage_ L2 - http://dx.doi.org/10.1097/00005344-200111002-00003 DB - PRIME DP - Unbound Medicine ER -