Abstract
Background. The renin-angiotensin system with its renal-humoral and local myocardial components plays an important role in the development and progression of chronic heart failure. Whereas angiotensin receptors have been found in atrial and ventricular myocardium of different species including humans, its influence on myocardial contractility is not yet defined in human failing myocardium and especially in human nonfailing myocardium. Methods and Results. We measured force development of right atrial and right and left ventricular myocardial preparations of patients with a variety of cardiac diseases. To evaluate the physiological effects of angiotensin, experimental temperature and stimulation rates were 37°C and 60 beats per minute, respectively. Angiotensin I and II increased peak developed force in atrial myocardial preparations obtained from patients without heart failure in a concentration-dependent manner. At optimal concentrations, peak developed force is increased from 10.2±1.8 to 12.3±1.9 mN/mm2 by angiotensin I (P
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Holubarsch, C., Hasenfuss, G., Schmidt-Schweda, S., Knorr, A., Pieske, B., Ruf, T., … Just, H. (1993). Angiotensin I and II exert inotropic effects in atrial but not in ventricular human myocardium an in vitro study under physiological experimental conditions. Circulation, 88(3), 1228–1237. https://doi.org/10.1161/01.CIR.88.3.1228
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