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This Article Full Text Full Text (PDF) All Versions of this Article: 289/2/H593    most recent 01240.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Santos, A. C. Articles by Negrão, C. E. Search for Related Content PubMed PubMed Citation Articles by Santos, A. C. Articles by Negrão, C. E.

Sympathetic activation restrains endothelium-mediated muscle vasodilatation in heart failure patients

¹Heart Institute, University of Sao Paulo Medical School, and ²Department of Physiology and Biophysics, Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, Brazil; ³Department of Cardiology, University of California, Los Angeles, California; and ⁴School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil

Submitted 8 December 2004 ; accepted in final form 11 March 2005

Although the vasodilatory response during mental stress is blunted in heart failure (HF), the mechanisms underlying this phenomenon are not fully understood. We tested the hypothesis that sympathetic activity limits the endothelium-dependent vasodilatation during mental stress in chronic HF patients. Twenty-one HF patients (age 45 ± 2 yr, functional classes III and IV, New York Heart Asssociation) and 22 age-matched normal controls (NC; age 42 ± 2 yr, P = 0.13) were studied at rest and during 4 min of Stroop color-word test with brachial intra-arterial saline, acetylcholine (endothelium dependent), phentolamine (-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 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 endothelium-mediated vasodilatation during mental stress in HF patients.

mental stress; forearm vasodilatation; endothelial function

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