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Growth dependent changes in the endothelial factors regulating arteriolar tone
Author(s) -
Samora Julie Balch,
Frisbee Jefferson C.,
Boegehold Matthew A.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a270
Subject(s) - weanling , medicine , endocrinology , dilator , simvastatin , arteriole , vasodilation , nitric oxide , acetylcholine , microcirculation , skeletal muscle , juvenile , chemistry , biology , genetics
Previous studies from our laboratory suggest that in young rats, the rapid growth of skeletal muscle and its vascular network is accompanied by a modification of the mechanisms responsible for the integrated regulation of blood flow. Building on this work, we studied isolated gracilis muscle arterioles from weanling (22–26 days) and juvenile (50–56 days) rats to test the hypothesis that this modification includes a change in the contribution of nitric oxide to the regulation of arteriolar tone. Normalized to dilator capacity, arteriolar responses to acetylcholine (ACh), A23187, VEGF and simvastatin were not different between age groups. Treatment with L‐NAME significantly attenuated the dilation to each of these agonists in juvenile, but not in weanling arterioles. In juvenile vessels, combined treatment with L‐NAME and indomethacin reduced ACh and simvastatin responses by 88–90% and 68–73%, respectively. In contrast, this combined treatment had no effect on responses to either agonist in weanling arterioles. Treatment with miconazole had no effect on ACh or simvastatin responses in either group. However, combined treatment with all three pathway inhibitors abolished ACh and simvastatin responses in juvenile arterioles, but had no consistent effect in weanling arterioles. These data suggest that age‐dependent differences in the control of vascular tone exist and may have significant implications for the regulation of tissue perfusion. (NIH RO1 DK64668, AHA 0330194N, NIH HL 44012)