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Mechanisms involved in angiotensin II induced increases in cardiac output in pithed rats.

This study was conducted to determine the mechanisms by which angiotensin II (Ang-II) acutely increases cardiac output. Pithed Sprague-Dawley rats were prepared for continuous measurement of cardiac output by electromagnetic flowmetry. Ang-II (31-1000 ng/kg, i.v.) produced dose-related increases in cardiac output, heart rate and stroke volume. Although the heart rate increases were abolished by beta-adrenoceptor blockade, the cardiac output responses were unchanged due to an offsetting increase in stroke volume. The constancy of the cardiac output response following beta-adrenoceptor blockade suggested that Ang-II increased cardiac output by constricting venous smooth muscle and thereby increasing venous return. This conclusion is supported by the observation that Ang-II produced marked increases in left ventricular end diastolic pressure that paralleled the increases in cardiac output. In fact, based on volume loading with Tyrode's solution, the changes in left ventricular end diastolic pressure produced by Ang-II should have resulted in even greater increases in cardiac output. However, it appears that the significant rise in peripheral resistance to Ang-II tended to counter the effects of increased venous return on cardiac output. In addition, the Ang-II-induced elevations in cardiac output were not altered by alpha-adrenoceptor blockade. Therefore, catecholamines do not play a role in mediating the Ang-II effects. The results of this study support the conclusion that Ang-II is capable of increasing cardiac output by constriction of venous smooth muscle.