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1 Department of Veterinary Biomedical Sciences, University of Missouri- Columbia, Columbia, Missouri 65211; and 2 Department of Health and Kinesiology, Texas A & M University, College Station, Texas 77843
Previous research
has shown that skeletal muscle blood flow, at rest and during muscular
contractions, is elevated in the hyperthyroid state. We hypothesized
that reduced vascular contractile and enhanced endothelium-dependent
relaxation responses contribute to these observations. To test these
hypotheses, male rats were administered triiodothyronine (Hyper,
n = 27; 300 µg/kg) for 6-12 wk.
Compared with euthyroid control rats (Eut,
n = 27), Hyper exhibited left
ventricular hypertrophy (Eut, 2.01 ± 0.04 mg/g body wt; Hyper, 2.70 ± 0.06; P < 0.0005) and greater
oxidative enzyme activity in several skeletal muscles (all
P < 0.0005). Vascular rings,
2-3 mm in axial length, were prepared from abdominal aortas, and
responses to vasoactive agents were determined in vitro. Compared with
Eut, vascular rings with intact endothelium from Hyper exhibited
reductions in contractile responses to norepinephrine (NE) across a
range of NE concentrations (P < 0.05). Maximal tension developed in response to NE was reduced ~30%
in hyperthyroidism (Eut, 3.8 ± 0.2 g; Hyper, 2.6 ± 0.4;
P < 0.01). Contractile responses to
NE were not different between Eut and Hyper in rings denuded of
endothelium. Maximal vasorelaxation responses to acetylcholine (ACh),
after precontraction with NE
(10
7 M), were enhanced in
the hyperthyroid state (Eut, 65.1 ± 4.8%; Hyper, 84.0 ± 7.1;
P < 0.05). Enhanced vasorelaxation
to ACh was also observed when precontraction was induced by
prostaglandin F2
. These
findings indicate that vascular contractile and relaxation responses
are altered in male hyperthyroid rats.
blood flow; smooth muscle; endothelium; norepinephrine; acetylcholine
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