Vol. 283, Issue 4, H1662-H1672, October 2002
Aging impairs endothelium-dependent vasodilation in rat
skeletal muscle arterioles
Judy M.
Muller-Delp1,
Scott A.
Spier1,
Michael
W.
Ramsey1, and
Michael D.
Delp1,2
Departments of 1 Health and Kinesiology and 2 Medical
Physiology, Texas A&M University, College Station, Texas 77843
Blood flow capacity in skeletal
muscle declines with age. Reduced blood flow capacity may be related to
decline in the maximal vasodilatory capacity of the resistance
vasculature. This study tested the hypothesis that aging results in
impaired vasodilatory capacity of first-order (1A) arterioles isolated
from rat-hindlimb locomotory muscle: 1A arterioles (90-220 µm)
from gastrocnemius and soleus muscles of young (4 mo) and aged (24 mo)
Fischer-144 rats were isolated, cannulated, and pressurized via
hydrostatic reservoirs. Vasodilatory responses to increasing
concentrations of ACh (10
9 to 10
4 M),
adenosine (ADO, 10
10 to 10
4 M), and sodium
nitroprusside (SNP, 10
10 to 10
4 M) were
evaluated at a constant intraluminal pressure of 60 cmH2O in the absence of flow. Flow-induced vasodilation was also evaluated in
the absence of pressure changes. Responses to ADO and SNP were not
altered by age. Endothelium-dependent vasodilation induced by flow was
significantly reduced in arterioles from both gastrocnemius and soleus
muscles. In contrast, endothelium-dependent vasodilation to ACh was
reduced only in soleus muscle arterioles. 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 soleus muscle
arterioles, suggesting that the mechanism of age-related endothelial
impairment differs in arterioles from soleus and gastrocnemius muscles.
acetylcholine; adenosine; nitric oxide; soleus; gastrocnemius; NG-nitro-L-arginine methyl ester; indomethacin