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Am J Physiol Regul Integr Comp Physiol 288: R284-R291, 2005. First published September 16, 2004; doi:10.1152/ajpregu.00061.2003
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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Thyroid status and endothelium-dependent vasodilation in skeletal muscle

R. M. McAllister,1 I. Albarracin,1 J. L. Jasperse,2 and E. M. Price3

1Departments of Anatomy and Physiology and Kinesiology, Kansas State University, Manhattan, Kansas; 2Department of Sports Medicine, Pepperdine University, Malibu, California; and 3Department of Veterinary Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri

Submitted 3 February 2003 ; accepted in final form 7 September 2004

Cardiovascular dysfunction is characteristic of both hypo- and hyperthyroidism. Endothelium-dependent dilation of conductance vessels is impaired in hypothyroidism but augmented in hyperthyroidism. We hypothesized that these alterations in dilation extend into the resistance vasculature of skeletal muscle. To test this hypothesis, rats were made hypothyroid with propylthiouracil (Hypo; n = 13) or hyperthyroid with triiodothyronine (Hyper; n = 9) over 3–4 mo. Compared with euthyroid controls (Eut; n = 14), Hypo rats were characterized by reduced skeletal muscle oxidative capacity and blunted growth; Hyper rats exhibited increased muscle oxidative capacity and left ventricular hypertrophy (P < 0.05 for all effects). Vasodilation to the endothelium-dependent agent acetylcholine (~2 x 10–4 M) in skeletal muscle was determined in situ. Conductance in certain muscles increased from control [e.g., soleus: 0.98 ± 0.15 (Eut), 0.79 ± 0.14 (Hypo), and 1.06 ± 0.24 ml·min–1·100 g–1·mmHg–1 (Hyper); not significant among groups] to acetylcholine [1.91 ± 0.21 (Eut), 2.28 ± 0.26 (Hypo), and 2.15 ± 0.33 ml·min–1·100 g–1·mmHg–1 (Hyper); P < 0.05 vs. control values for all groups] but did not differ among groups. Expression of mRNA for the endothelial isoform of nitric oxide synthase in resistance vessels isolated from various muscles was similarly unchanged with alterations in thyroid status [e.g., soleus 1A arterioles: 33.15 ± 0.58 (Eut), 32.73 ± 0.27 (Hypo), and 32.80 ± 0.54 (Hyper) cycles at threshold; not significant]. These data suggest that endothelium-dependent dilation of resistance vasculature in skeletal muscle is unchanged in both hypo- and hyperthyroidism. These data also emphasize the importance of examining resistance vasculature to improve understanding of effects of chronic disease on integrated cardiovascular function.

hypothyroidism; hyperthyroidism; acetylcholine; muscle fiber type; nitric oxide synthase



Address for reprint requests and other correspondence: R. M. McAllister, Dept. of Anatomy and Physiology, Kansas State Univ., 228 Coles Hall, Manhattan, KS 66506 (E-mail: mcallist{at}vet.ksu.edu)




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D. G. Ingram, S. C. Newcomer, E. M. Price, K. E. Eklund, R. M. McAllister, and M. H. Laughlin
Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles
Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2798 - H2808.
[Abstract] [Full Text] [PDF]




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