Abstract

Recent studies have shown that the infusion of atriopeptins decreases blood volume because of the diuresis and also because of changes in vascular volume. In dogs chronically instrumented for the measurement of left ventricular pressure and internal left ventricular diameter, infusion of atriopeptin 24 (500 ng.kg-1.min-1 for 1 h), steady-state plasma levels of 6,000 pg/ml resulted in 5.9 +/- 1.7% decrease in left ventricular (LV) end-diastolic diameter (EDD) from 34.7 +/- 2.3 mm (P less than 0.05) and no significant change in LV first derivative of pressure with time (dP/dt), LV first derivative of dimension with time, LV dP/dt divided by internal diastolic circumference or percent shortening. Hematocrit increased from 42 to 46% (P less than 0.05). During pacing, infusion of atriopeptin 24 still reduced LV EDD by 7.5 +/- 1.8% from 32 +/- 2.8 mm (P less than 0.05), although there were no changes in the indexes of inotropic state. These results were unaffected by combined autonomic receptor blockade or by ganglionic blockade. Inflation of a hydraulic occluder around the aorta during the infusion of atriopeptin 24 to return LV EDD to preinfusion levels did not cause any index of myocardial contractility to increase significantly. At lower infusion rates that resulted in plasma atriopeptin levels of 2,000 pg/ml, atriopeptin 24 still reduced LV EDD without effect on inotropic state. Thus in the conscious dog, atriopeptins reduce preload independent of neuronal influences and without affecting inotropic state.

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