Sympathetic nerve responses to muscle contraction and stretch in ischemic heart failure

2008 ◽  
Vol 294 (1) ◽  
pp. H311-H321 ◽  
Author(s):  
Satoshi Koba ◽  
Jihong Xing ◽  
Lawrence I. Sinoway ◽  
Jianhua Li

Congestive heart failure (CHF) induces abnormal regulation of peripheral blood flow during exercise. Previous studies have suggested that a reflex from contracting muscle is disordered in this disease. However, there has been very little investigation of the muscle reflex regulating sympathetic outflows in CHF. Myocardial infarction (MI) was induced by the coronary artery ligation in rats. Echocardiography was performed to determine fractional shortening (FS), an index of the left ventricular function. We examined renal and lumbar sympathetic nerve activities (RSNA and LSNA, respectively) during 1-min repetitive (1- to 4-s stimulation to relaxation) contraction or stretch of the triceps surae muscles. During these interventions, the RSNA and LSNA responded synchronously as tension was developed. The RSNA and LSNA responses to contraction were significantly greater in MI rats ( n = 13) with FS <30% than in control animals ( n = 13) with FS >40% (RSNA: +49 ± 7 vs. +19 ± 4 a.u., P < 0.01; LSNA: +28 ± 7 vs. +8 ± 2 a.u., P < 0.01) at the same tension development. Stretch also increased the RSNA and LSNA to a larger degree in MI ( n = 13) than in control animals ( n = 13) (RSNA: +36 ± 6 vs. +19 ± 3 a.u., P < 0.05; LSNA: +24 ± 3 vs. +9 ± 2 a.u., P < 0.01). The data demonstrate that CHF exaggerates sympathetic nerve responses to muscle contraction as well as stretch. We suggest that muscle afferent-mediated sympathetic outflows contribute to the abnormal regulation of peripheral blood flow seen during exercise in CHF.

2010 ◽  
Vol 298 (5) ◽  
pp. H1438-H1444 ◽  
Author(s):  
Satoshi Koba ◽  
Jihong Xing ◽  
Lawrence I. Sinoway ◽  
Jianhua Li

Previous animal and human studies have suggested that a muscle reflex engaged during contraction leads to heightened levels of sympathetic activity in congestive heart failure (CHF). The present experiment was designed to test the role for bradykinin, which is produced within contracting skeletal muscle and contributes to the muscle reflex through its action on kinin B2 receptors located on the endings of thin fiber muscle afferents. CHF was induced in rats by myocardial infarction (MI) after coronary artery ligation. Echocardiography was performed to determine fractional shortening (FS), an index of the left ventricular function. In the decerebrate rats, we examined renal sympathetic nerve activity (RSNA) during 1 min intermittent (1 to 4 s stimulation to relaxation) contraction of left triceps surae muscles. RSNA responded synchronously as tension was developed, and the response was significantly ( P < 0.05) greater in MI rats [+39 ± 9% s−1 (integrated RSNA over time); n = 16] with 20 ± 2% of FS than that in control healthy rats (+19 ± 2% s−1; n = 16) with 49 ± 2% of FS. Tension development did not differ significantly between the two groups of rats. Thirty minutes after intra-arterial injection into the hindlimb circulation of the kinin B2 receptor antagonist, HOE-140 (2 μg/kg), the RSNA response to contraction was significantly reduced in the MI rats (+26 ± 7% s−1) but not in the control rats (+17 ± 2% s−1). These data suggest that bradykinin within contracting muscle is part of the exaggerated muscle reflex seen in CHF.


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