Abstract 16533: Exercise Training Normalizes Renal Blood Flow Responses to Acute Hypoxia and Exercise in Experimental Heart Failure
Chronic heart failure (CHF) is often accompanied by a decrease in renal function. The mechanisms of the cardio-renal syndrome are unclear. Exercise training (ExT) has been shown to be a non-pharmacologic therapy in the CHF state. We hypothesized that ExT in the CHF state would ameliorate the renal vasoconstrictor response to two important stressors. CHF was induced in rabbits by chronic ventricular pacing and assessed by echocardiography. Animals were randomly divided into an ExT or sedentary (SED) group. ExT was carried out for 3 weeks during the pacing period. SED rabbits were studied during the same time frame. Before and after ExT or the SED period the responses to a 5 minute treadmill exercise challenge and to 6 minutes of 5% O2 breathing were assessed. Renal blood flow (RBF), heart rate and arterial pressure were continuously recorded by chronic instrumentation. CHF SED rabbits exhibited approximately a 35% decrease in baseline RBF (n=5; 48.6±4.1 ml/min pre paced vs. 31.6±3.2 ml/min post paced; p<0.001). ExT increased baseline RBF to 42.4±4.3 ml/min (n=7; p=0.067 compared to SED rabbits). Acute hypoxia reduced RBF to 5.0±3.3 ml/min during the first 2 minutes with a recovery to 25.0±5.5 ml/min over the subsequent 4 minutes in pre paced rabbits. In SED CHF rabbits RBF decreased comparably within the first 2 minutes but increased at a slower rate during the subsequent 4 minutes (p<0.05 between minutes 3.5 and 5.5). However, ExT ameliorated the responses to hypoxia in CHF rabbits (p<0.05 at minutes 3.5, 4 and 5.5 compared to SED rabbits). Systemic administration of prazosin removed the differences in RBF between CHF SED and ExT rabbits. An acute exercise challenge reduced RBF in CHF SED rabbits to a greater extent than in pre paced rabbits (p<0.05) at all time points. This response was normalized following ExT (see figure). These results suggest that ExT reduces renal vasoconstrictor response to acute stress in CHF, most likely via a reduction in renal sympathetic nerve activity.
- © 2011 by American Heart Association, Inc.