Home > Riviste > International Angiology > Fascicoli precedenti > International Angiology 2009 December;28(6) > International Angiology 2009 December;28(6):474-8

ULTIMO FASCICOLO
 

ARTICLE TOOLS

Estratti

INTERNATIONAL ANGIOLOGY

Rivista di Angiologia


Official Journal of the International Union of Angiology, the International Union of Phlebology and the Central European Vascular Forum
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,37


eTOC

 

Original articles  


International Angiology 2009 December;28(6):474-8

Copyright © 2010 EDIZIONI MINERVA MEDICA

lingua: Inglese

Thyroid hormone modulates the responsiveness of rat aorta to a1-adrenergic stimulation: an effect due to increased activation of b2-adrenergic signaling

Pappas M., Mourouzis K., Karageorgiou H., Tes-seromatis C., Mourouzis I., Kostopanagiotou G., Pantos C., Cokkinos D. V.

1 Department of Pharmacology, University of Athens, Athens, Greece; 2 1st Cardiology Department, Onassis Cardiac Surgery Center, Athens, Greece


PDF  


AIM:The ability of the thyroid hormone to increase cardiac output and to lower systemic vascular resistance may provide a novel treatment for cardiovascular diseases. Therefore, understanding the mechanisms of thyroid hormone action on the heart and peripheral vasculature could be of clinical importance. We previously found that thyroid hormone modulates the a1-adrenergic effect on vascular reactivity of rat aortas. In the present study we further investigated possible mechanisms of this response.
METHODS: Hyperthyroidism was induced on Wistar -Kyoto male rats with L-Thyroxine, (THYR) treatment for two weeks, N.=18 while untreated rats used as controls (NORM), N.=16. The thoracic aorta was dissected and cut into rings that were suspended in an isolated organ bath with Krebs-Henseleit buffer. Maximal tension, Tmax, in g was measured in response to Potassium Chloride (KCl) and Phenylephrine (PE) in rings in the presence of Ritodrine, a b-2 agonist (NORM-RITO, N:=8, THYR-RITO, N.=9), or in the absence of Ritodrine (THYR, N.=9, NORM, N.=8).
RESULTS: With KCL, Tmax was not different between the THYR, NORM, NORM-RITO, and THYR-RITO groups. With PE, there was a difference in Tmax between NORM-RITO and NORM, 0.66 (0.056) g vs 1.00 (0.066) g, P<0.05 and THYR and NORM, 0.75 (0.055) g vs 1.00 (0.066) g, P<0.05. No significant difference was observed between THYR-RITO AND THYR. Furthermore, Relax % was not significantly different between the NORM and the THYR, NORM-RITO, and THYR-RITO groups, 64.5%(3.7) vs 67.3%(6.7), 73.5% (4.3) and 81.8 %(4.7), P>0.05.
CONCLUSIONS: PE induced vasoconstriction in isolated rat aortic rings was reduced after both ritodrine and thyroxine treatment. However, co-administration of thyroid hormone and ritodrine did not result in a synergistic reduction of PE induced vasoconstriction. Thus, thyroxine may modulate the ·1-adrenergic vascular responsiveness by enhancing ‚2-adrenergic stimulation.

inizio pagina

Publication History

Per citare questo articolo

Corresponding author e-mail

cpantos@cc.uoa.gr