Submitted on December 8, 2004
Accepted on March 11, 2005
Sympathetic Activation Restrains Endothelial-Mediated Muscle Vasodilatation in Heart Failure Patients
Amilton C Santos1, Maria Janieire N Alves2, Maria Urbana P Rondon2, Antonio Carlos P Barretto2, Holly R Middlekauff3, and Carlos E Negrao4*
1 Unit of Cardiovascular Rehabilitation and Exercise Physiology, Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, SP, Brazil; Department of Physiology and Biophysics, Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, SP, Brazil
2 Unit of Cardiovascular Rehabilitation and Exercise Physiology, Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, SP, Brazil
3 Department of Cardiology, University of California Los Angeles, Los Angeles, CA, USA
4 Unit of Cardiovascular Rehabilitation and Exercise Physiology, Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, SP, Brazil; School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, SP, Brazil
* To whom correspondence should be addressed. E-mail: cndnegrao{at}incor.usp.br.
Although the vasodilatory response during mental stress is blunted in heart failure, the mechanisms underlying this phenomenon are not fully understood. We tested the hypothesis that sympathetic activity limits the endothelial-dependent vasodilatation during mental stress in chronic heart failure (HF) patients. Twenty-one HF patients (age 45 ± 2 years, Functional Class III-IV, NYHA), and 22 age-matched normal controls (NC, age 42 ± 2 years, P=0.13) were studied at rest and during 4 minutes of Stroop color word test with brachial intra-arterial saline, acetylcholine (endothelial-dependent), phentolamine (alpha-blocker), and phentolamine plus acetylcholine infusion. Forearm blood flow was measured by venous occlusion plethysmography. Baseline forearm vascular conductance (FVC) was significantly lower in HF patients (2.18 ± 0.12 vs. 3.66 ± 0.22 units, P=0.001). During mental stress with saline, the changes in FVC were significantly blunted in HF patients when compared with NC (0.92 ± 0.20 vs. 2.13 ± 0.39 units, P=0.001). In HF, the vasodilatation with acetylcholine was similar to saline control and significantly lower than in NC. In HF patients, phentolamine significantly increased FVC responses (1.16 ± 0.20 vs. 2.09 ± 0.29 units, P=0.001), and the difference between HF patients and NC tended to decrease (2.09 ±0.29 vs. 3.61 ± 0.74 units, P=0.052). The vasodilatation with phentolamine plus acetylcholine was similar between HF and NC (4.23 ± 0.73 vs. 4.76 ± 1.03 units, P=0.84). In conclusion, sympathetic activation mediates the blunted muscle endothelially-mediated vasodilatation during mental stress in HF patients.
