Modulation of sympathetic control by ACE inhibitors

P Dominiak ¹

⁰Institute of Pharmacology, Medical University of Lübeck, Germany.

European Heart Journal +

|

November 1, 1993

View abstract on PubMed

Summary

Angiotensin-converting enzyme (ACE) inhibitors affect catecholamine release. Bradykinin, influenced by ACE inhibitors, stimulates noradrenaline release, potentially compensating for ACE inhibitors' direct effects.

Area Of Science

Pharmacology
Cardiovascular Physiology
Neuroendocrinology

Background

Angiotensin-converting enzyme (ACE) inhibitors modulate the renin-angiotensin-aldosterone system.
ACE also metabolizes bradykinin, a peptide that influences catecholamine release.
Potential indirect effects of ACE inhibitors on sympathetic nervous system function are not fully understood.

Purpose Of The Study

To investigate the impact of ACE inhibition on catecholamine (noradrenaline and adrenaline) release.
To examine the role of angiotensin I and bradykinin in modulating catecholamine release during ACE inhibition.
To assess the effect of ramipril, an ACE inhibitor, on noradrenaline reuptake.

Main Methods

Evaluation of catecholamine biosynthesis, storage, and release under chronic ACE inhibition.
Assessment of noradrenaline reuptake mechanisms in the presence of ramipril.
Dose-dependent studies of angiotensin I and bradykinin effects on noradrenaline release during ACE inhibition.

Main Results

Chronic ACE inhibition did not alter catecholamine biosynthesis, storage, or release.
Ramipril significantly diminished noradrenaline reuptake.
Bradykinin, but not angiotensin I, dose-dependently stimulated noradrenaline release during ACE inhibition.

Conclusions

ACE inhibitors do not directly affect catecholamine release but can alter noradrenaline reuptake.
Bradykinin plays a significant role in modulating noradrenaline release under ACE inhibition.
Bradykinin may compensate for the lack of direct effect of ACE inhibitors on catecholamine release.

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