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Articles in PresS, published online ahead of print June 20, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00004.2002
Submitted on January 3, 2002
Accepted on June 18, 2002
1 Department of Health and Kinesiology, Texas A&M University, College Station, TX, Texas, USA
2 Department of Health and Kinesiology, Texas A&M University, College Station, TX, Texas, USA; Department of Medical Physiology, Texas A&M Health Science Center, College Station, Texas, USA
* To whom correspondence should be addressed. E-mail: jmd{at}hlkn.tamu.edu.
Blood flow capacity in skeletal muscle declines with age. A reduction in blood flow capacity may be related to a decline in the maximal vasodilatory capacity of the resistance vasculature. The purpose of this study was to test the hypothesis that aging results in impaired vasodilatory capacity of 1A arterioles isolated from locomotory muscle of the rat hindlimb. First order (1A) arterioles (90-220 µm) from gastrocnemius and soleus muscles of young (4 months) and aged (24 months) Fischer rats were isolated, cannulated, and pressurized via hydrostatic reservoirs. Vasodilatory responses to increasing concentrations of acetylcholine (Ach; 1x10-9-1x10-4 M), adenosine (ADO; 1x10-10-1x10-4 M), and sodium nitroprusside (SNP; 1x10-10-1x10-4 M) were evaluated at a constant intraluminal pressure of 60 cm H2O in the absence of flow. Flow-induced vasodilation was also evaluated in the absence of pressure changes. Responses to adenosine and sodium nitroprusside were not altered by age. Endothelium-dependent vasodilation induced by flow was significantly reduced in arterioles from both the gastrocnemius and soleus muscles. In contrast, endothelium-dependent vasodilation to acetylcholine was reduced only in arterioles from the soleus muscle. These results indicate that aging impairs vasodilatory responses mediated through the endothelium of resistance arterioles from locomotory muscle, whereas smooth muscle vasodilatory responses remain intact with aging. Additionally, Ach-induced vasodilation was altered by age only in arterioles from soleus muscle suggesting that the mechanism of age-related endothelial impairment differs in arterioles from soleus and gastrocnemius muscles.
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