Abstract
In young rats, skeletal muscle arterioles respond to acetylcholine, which elicits Ca2+-dependent endothelial nitric oxide (NO) release, but not to shear stress, which does not require increased intracellular Ca2+ for endothelial NO release. The aim of this study was to determine if, in general, signaling pathways for endothelial NO release that differ in their reliance on Ca2+ may be developing at different times during normal arteriolar network growth in skeletal muscle. Arteriolar responses to intraluminal infusion of the Ca2+ ionophore A23187, and the Ca2+-independent agonists vascular endothelial growth factor (VEGF) and simvastatin, were studied before and during NO synthase (NOS) inhibition with NG-monomethyl-L-arginine (L-NMMA) in the exteriorized spinotrapezius muscle of weanling (age 4-5 wks) and juvenile (7-8 wks) rats. There were no age-dependent differences in arteriolar responses to A23187 applied over a concentration range that dilated arterioles from 9 +/- 2 to 74 +/- 8% of maximum, and L-NMMA attenuated these responses by the same amount in both age groups. In juveniles, arterioles dilated up to 39+/-5% of maximum in response to VEGF, and up to 83 +/- 6% of maximum in response to simvastatin, with L-NMMA greatly...Continue Reading
Citations
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