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(Circulation. 2000;101:784.)
© 2000 American Heart Association, Inc.

Clinical Investigation and Reports

Exaggerated Renal Vasoconstriction During Exercise in Heart Failure Patients

Holly R. Middlekauff, MD; Egbert U. Nitzsche, MD; Carl K. Hoh, MD; Michele A. Hamilton, MD; Gregg C. Fonarow, MD; Antoine Hage, MD; Jaime D. Moriguchi, MD

From the Division of Cardiology, Department of Medicine, and Division of Nuclear Medicine and Biophysics, Department of Pharmacology, UCLA School of Medicine, Los Angeles, Calif. Dr Nitzsche is now at the Division of Nuclear Medicine and Biophysics, Albert-Ludwigs-University, School of Medicine, Freiburg, Germany.

Correspondence to Holly R. Middlekauff, MD, UCLA Department of Medicine, Division of Cardiology, 47-123 CHS, 10833 Le Conte Ave, Los Angeles, CA 90095.

Background—During static exercise in normal healthy humans, reflex renal cortical vasoconstriction occurs. Muscle metaboreceptors contribute importantly to this reflex renal vasoconstriction. In patients with heart failure, in whom renal vascular tone is already increased at rest, it is unknown whether there is further reflex renal vasoconstriction during exercise.

Methods and Results—Thirty-nine heart failure patients (NYHA functional class III and IV) and 38 age-matched control subjects (controls) were studied. Renal blood flow was measured by dynamic positron emission tomography. Graded handgrip exercise and posthandgrip ischemic arrest were used to clarify the reflex mechanisms involved. During sustained handgrip (30% maximum voluntary contraction), peak renal vasoconstriction was significantly increased in heart failure patients compared with controls (70±13 versus 42±1 U, P=0.02). Renal vasoconstriction returned to baseline in normal humans by 2 to 5 minutes but remained significantly increased in heart failure patients at 2 to 5 minutes and had returned to baseline at 20 minutes. In contrast, during posthandgrip circulatory arrest, which isolates muscle metaboreceptors, peak renal vasoconstriction was not greater in heart failure patients than in normal controls. In fact, the increase in renal vasoconstriction was blunted in heart failure patients compared with controls (20±5 versus 30±2 U, P=0.05).

Conclusions—During sustained handgrip exercise in heart failure, both the magnitude and duration of reflex renal vasoconstriction are exaggerated in heart failure patients compared with normal healthy humans. The contribution of the muscle metaboreceptors to reflex renal vasoconstriction is blunted in heart failure patients compared with normal controls.

Key Words: exercise • heart failure • vasoconstriction • kidney

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