| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of Anatomy and Physiology and Kinesiology, Kansas State University, Manhattan, Kansas 66506, USA
1 Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA
(Requests for offprints should be addressed to R M McAllister, Department of Anatomy and Physiology, Kansas State University, 228 Coles Hall, Manhattan, Kansas 66506, USA; Email: mcallist{at}vet.ksu.edu)
Thyroid disease has profound effects on cardiovascular function. Hypo- and hyperthyroidism, for example, are associated with reduced and increased maximal endothelium-dependent vasodilation respectively. We therefore hypothesized that the capacity for vascular nitric oxide (NO) formation is decreased in hypothyroidism and increased in hyperthyroidism. To test this hypothesis, rats were made hypothyroid (HYPO) with propylthiouracil or hyperthyroid (HYPER) with triiodothyronine over 3–4 months. Compared with euthyroid control rats (EUT), HYPO exhibited blunted growth and lower citrate synthase activity in the soleus muscle; HYPER exhibited left ventricular hypertrophy and higher citrate synthase activity in the soleus muscle (P<0.05 for all effects). The capacity for NO formation was determined in aortic extracts by formation of [3H]L-citrulline from [3H]L-arginine, i.e. NO synthase (NOS) activity. Thyroid status modulated NOS activity (EUT, 36.8 ± 5.5 fmol/h per mg protein; HYPO, 26.0 ± 7.9; HYPER, 64.6 ± 12.7; P<0.05, HYPER vs HYPO). Expression of endothelial and neural isoforms of NOS was modulated by thyroid status in a parallel fashion. Capacity for responding to NO was also determined via measuring cGMP concentration in aortae incubated with sodium nitroprusside. Stimulated cGMP formation was also modulated by thyroid status (EUT, 73.0 ± 20.2 pmol/mg protein; HYPO, 152.4 ± 48.7; HYPER, 10.4 ± 2.6; P<0.05, HYPER vs HYPO). These data indicate that thyroid status alters capacities for both formation of and responding to NO. The former finding may contribute to previous findings concerning vascular function in thyroid disease states.
This article has been cited by other articles:
|
|
 |
|
  M. A. Carrillo-Sepulveda, G. S. Ceravolo, Z. B. Fortes, M. H. Carvalho, R. C. Tostes, F. R. Laurindo, R. C. Webb, and M. L. M. Barreto-Chaves Thyroid hormone stimulates NO production via activation of the PI3K/Akt pathway in vascular myocytes Cardiovasc Res, February 1, 2010; 85(3): 560 - 570. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Biondi, M. Galderisi, L. Pagano, M. Sidiropulos, M. Pulcrano, A. D' Errico, S. Ippolito, A. Rossi, O. de Divitiis, and G. Lombardi Endothelial-mediated coronary flow reserve in patients with mild thyroid hormone deficiency Eur. J. Endocrinol., August 1, 2009; 161(2): 323 - 329. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Volzke, D. M. Robinson, T. Spielhagen, M. Nauck, A. Obst, R. Ewert, B. Wolff, H. Wallaschofski, S. B. Felix, and M. Dorr Are serum thyrotropin levels within the reference range associated with endothelial function? Eur. Heart J., January 2, 2009; 30(2): 217 - 224. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. D. Owen, C. Rajiv, D. Vinereanu, T. Mathew, A. G. Fraser, and J. H. Lazarus Subclinical Hypothyroidism, Arterial Stiffness, and Myocardial Reserve J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2126 - 2132. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-D. Tang, J. A. Kuzman, S. Said, B. E. Anderson, X. Wang, and A. M. Gerdes Low Thyroid Function Leads to Cardiac Atrophy With Chamber Dilatation, Impaired Myocardial Blood Flow, Loss of Arterioles, and Severe Systolic Dysfunction Circulation, November 15, 2005; 112(20): 3122 - 3130. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
