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1 Division of Cardiology, Department of Medicine, University of California, Los Angeles, California 90095; and 2 Division of Nuclear Medicine, Department of Radiology, University of Basel, School of Medicine and Medical Center, CH-4031 Basel, Switzerland
In heart failure (HF)
patients, reflex renal vasoconstriction during exercise is
exaggerated. We hypothesized that muscle mechanoreceptor
control of renal vasoconstriction is exaggerated in HF. Nineteen HF
patients and nineteen controls were enrolled in two exercise protocols:
1) low-level rhythmic handgrip (mechanoreceptors and central
command) and 2) involuntary biceps contractions
(mechanoreceptors). Renal cortical blood flow was measured by
positron emission tomography, and renal cortical vascular resistance
(RCVR) was calculated. During rhythmic handgrip, peak RCVR was greater
in HF patients compared with controls (37 ± 1 vs. 27 ± 1 units; P < 0.01). Change in (
) RCVR tended to be
greater as well but did not reach statistical significance (10 ± 1 vs. 7 ± 0.9 units; P = 0.13). RCVR was
returned to baseline at 2-3 min postexercise in controls but
remained significantly elevated in HF patients. During
involuntary muscle contractions, peak RCVR was greater in HF
patients compared with controls (36 ± 0.7 vs. 24 ± 0.5 units; P < 0.0001). The RCVR was also
significantly greater in HF patients compared with controls (6 ± 1 vs. 4 ± 0.6 units; P = 0.05). The data suggest
that reflex renal vasoconstriction is exaggerated in both magnitude and
duration during dynamic exercise in HF patients. Given that the
exaggerated response was elicited in both the presence and absence of
central command, it is clear that intact muscle mechanoreceptor
sensitivity contributes to this augmented reflex renal vasoconstriction.
exercise; sympathetic nervous system; renal circulation; congestive heart failure
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