Modulation of sympathetic control by ACE inhibitors.
ACE inhibitors may influence the actual concentrations of the peptides angiotensin I, angiotensin II and bradykinin. Since all three peptides are able to modulate catecholamine release, a change in noradrenaline and adrenaline release should be expected when angiotensin I converting enzyme (kininase II) is inhibited. Furthermore, converting enzyme inhibitors may also act indirectly on sympathetic membranes affecting, for instance, the reuptake mechanism of noradrenaline. It was shown that chronic ACE inhibition did not change biosynthesis, storage or release of catecholamines. However, the reuptake of noradrenaline was slightly but significantly diminished by ramipril. Whereas Ang I exerted no facilitating action on noradrenaline, bradykinin stimulated noradrenaline release dose-dependently, almost during converting enzyme inhibition. It is concluded that bradykinin may compensate for the lack of effect of converting enzyme inhibitors on catecholamine release.
Dominiak
P
P
Institute of Pharmacology, Medical University of Lübeck, Germany.
D000803:Angiotensin I / Q000502:physiology; D000804:Angiotensin II / Q000502:physiology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001920:Bradykinin / Q000502:physiology; D004837:Epinephrine / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; D000803:Angiotensin I; D001920:Bradykinin; D009638:Norepinephrine; D004837:Epinephrine