September 1, 1993Circulation
Angiotensin I and II exert inotropic effects in atrial but not in ventricular human myocardium. An in vitro study under physiological experimental conditions.
Why the study?
Do Angiotensin I and II increase peak developed force in human atrial and ventricular myocardial preparations?
Population
Right atrial and right and left ventricular myocardial preparations from patients with a variety of cardiac…
Comparison
Angiotensin I and II vs Baseline/control
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Does not support direct ventricular inotropy from angiotensin II; leaves open atrial-specific local ACE effects in vivo.
Key Points
- To determine the direct contractile effects of angiotensin I and II on human atrial and ventricular myocardium under physiological experimental conditions.
- Measured isometric force development in isolated human right atrial and right/left ventricular tissue preparations stimulated at 60 beats per minute at 37°C.
- Tested concentration-dependent responses to angiotensin I and II in nonfailing and failing myocardium alongside blockers including propranolol, prazosin, saralasin, and enalaprilat.
- Angiotensin I and II increased peak developed force in nonfailing atrial tissue from 10.2 ± 1.8 to 12.3 ± 1.9 mN/mm² (P < .05) and 15.4 ± 2.1 to 20.5 ± 3.3 mN/mm² (P < .05), respectively.
- Atrial contractile responses were completely blocked by saralasin (10⁻⁶ mol/L) and enalaprilat (10⁻⁵ mol/L for angiotensin I), but were unaffected by adrenergic blockade with propranolol and prazosin.
- Neither angiotensin I nor angiotensin II produced any inotropic response in right or left ventricular preparations across nonfailing hearts, dilated cardiomyopathy, mitral valve disease, or tetralogy of Fallot.
Structured PICO
Do Angiotensin I and II increase peak developed force in human atrial and ventricular myocardial preparations?
P
Population
Right atrial and right and left ventricular myocardial preparations from patients with a variety of cardiac diseases (idiopathic dilated cardiomyopathy, mitral valve stenosis and incompetence, no significant heart disease, tetralogy of Fallot)
I
Intervention
Angiotensin I and II
C
Comparator
Baseline/control
O
Outcome
Peak developed force (myocardial contractility)surrogate
Angiotensin I and II exert positive inotropic effects in human atrial myocardium but not in ventricular myocardium, demonstrating the functional importance of local myocardial angiotensin converting enzyme.
Cite This Study
Holubarsch et al. (1993) studied this question.