Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2010; Volume 198, Supplement 677
Joint Meeting of the Scandinavian and German Physiological Societies
3/27/2010-3/30/2010
Copenhagen, Denmark


THE -2-ADRENOCEPTOR AGONIST TERBUTALINE SPECIFICALLY DECREASES PULMONARY ARTERIAL PRESSURE BY -ADRENOCEPTOR ANTAGONISM
Abstract number: P-TUE-1

WENZEL1 D, STOLLE1 V, KNIES1 R, MATTHEY1 M, WELSCHOFF1 J, BREUER1 J, FLEISCHMANN1 BK

Objectives: b2-adrenoceptor agonists are important bronchodilators in the treatment of obstructive lung disease. In the present study we investigated the impact of the b2- adrenoceptor agonist terbutaline on pulmonary arterial pressure. Methods: The effect of terbutaline on vascular tone was measured in dose- response curves after precontraction with different vasoconstrictors in a wire-myograph. The results were confirmed in lung slices and in the isolated perfused lung model of mouse. Results: Terbutaline decreased the arterial tone of pulmonary arteries but not aortas in a dose- dependent manner after precontraction with phenylephrine and serotonin; this effect was neither observed after pre-treatment with endothelin nor the thromboxane agonist U46619. Further experiments proved that vasorelaxation by terbutaline was independent from the endothelium and the eNOS/NO pathway. Interestingly, b1- and b2-adrenoceptor inhibitors had no impact on terbutaline-induced vasodilation in pulmonary artery. However, treatment with the b1-adrenoceptor inhibitor phentolamin and Schild-plot analyses revealed that terbutaline acts as an antagonist at b-adrenoceptors and thereby relaxes pulmonary arteries. Vasorelaxation by terbutaline was found to be physiologically relevant as it occurred in both, large pulmonary artery and small vessels of lung slices as well as in the isolated perfused lung model. Conclusion: We conclude that besides its bronchodilating effect terbutaline specifically decreases pulmonary arterial vascular tone. This pharmacological action could be an interesting therapeutic option for the treatment of pulmonary arterial hypertension.

To cite this abstract, please use the following information:
Acta Physiologica 2010; Volume 198, Supplement 677 :P-TUE-1

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE