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Effects of angiotensin II on myocardial contractility during short‐term pressor responses to angiotensin II

Background Cardiac angiotensin AT1 receptors have been found in several animal species. In-vitro studies performed on cardiac preparations have shown that angiotensin II (ANG II) exerts a positive inotropic effect; however, in-vivo results have allowed no definitive conclusion to be drawn. The reasons behind these controversial results remain unknown, and could originate both from different experimental conditions and from the techniques used to assess myocardial contractility. Objective To investigate, by means of echocardiographic measurements, whether ANG II, administered to intact and to sinoaortic denervated isoflurane-anesthetized rabbits, was able to directly increase myocardial contractility. Methods The effect of ANG II on cardiac contractility was assessed with the use of simultaneous pressure measurements and Doppler-echocardiographic recordings. Specifically, we used both the relationship between the left ventricular end-systolic wall stress and the velocity of heart-rate-corrected circumferential fiber shortening (VCFC) and the maximum rate of rise of the ventricular pressure as indices of changes in myocardial contractility. Cardiac contractility was evaluated both in intact and in chronically sinoaortic denervated isoflurane-anesthetized rabbits under basal conditions and after ANG II infusion (50 ng/kg per min). Results After ANG II infusion, increases in mean arterial blood pressure, left ventricular end-diastolic diameter and pressure were observed both in intact and in chronically sinoaortic denervated rabbits. The left ventricular end-systolic wall stress (a function of the mean arterial pressure and chamber size) and the maximum rate of rise of the ventricular pressure rose markedly in rabbits of both groups, whereas the VCFC decreased significantly. However, when we compared the VCFC under ANG II infusion with that calculated at the same level of left ventricular afterload under basal conditions, we observed that ANG II infusion induced no significant change in VCFC either in intact or in chronically sinoaortic denervated rabbits. Conclusion Our results indicate that administration of ANG II to isoflurane-anesthetized rabbits induces a marked rise in ventricular pre- and after-loads and exerts no significant effect on the cardiac contractility. In light of this, it is reasonable to assume that the short-term increase in arterial blood pressure can be ascribed mainly to the increase in peripheral arterial resistance.