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Am J Physiol Heart Circ Physiol (January 21, 2005). doi:10.1152/ajpheart.00354.2004
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Submitted on April 13, 2004
Accepted on January 16, 2005

Sympathetic innervation promotes vascular smooth muscle differentiation

Deborah H Damon1*

1 Pharmacology, University of Vermont, Burlington, VT, USA

* To whom correspondence should be addressed. E-mail: Deborah.Damon{at}uvm.edu.

The sympathetic nervous system (SNS) is an important modulator of vascular smooth muscle (VSM) growth and function. Several lines of evidence suggest that the SNS also promotes VSM differentiation. The present study tests this hypothesis. Expression of smooth muscle myosin (SM2) and {alpha}-actin were assessed by western analysis as indices of VSM differentiation. SM2 expression (normalized to {alpha}-actin) in adult innervated rat femoral and tail arteries was 479 ± 115% of that in non-innervated carotid arteries. Alpha actin expression (normalized to GAPDH or total protein) in 30 day innervated rat femoral arteries was greater than that in corresponding non-innervated femoral arteries from guanethidine-sympathectomized rats. SM2 expression (normalized to {alpha} actin) in neonatal femoral arteries grown in vitro for 7 days in the presence of sympathetic ganglia was greater than SM2 expression in corresponding arteries grown in the absence of sympathetic ganglia. Alpha actin (normalized to GAPDH) in VSM/endothelial cell cultures grown in the presence of dissociated sympathetic neurons was 300 ± 66% of that in corresponding cultures grown in the absence of neurons. This effect was inhibited by an antibody that neutralized the activity of transforming growth factor {beta}2. All of these data indicate that sympathetic innervation increased VSM contractile protein expression and thereby suggest that the SNS promotes and/or maintains VSM differentiation.




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