HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 544/3/913    most recent 2002.030478v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Markos, F. Articles by Snow, H. M. Search for Related Content PubMed PubMed Citation Articles by Markos, F. Articles by Snow, H. M.

The effect of tezosentan, a non-selective endothelin receptor antagonist, on shear stress-induced changes in arterial diameter of the anaesthetized dog

F. Markos, B. A. Hennessy, M. Fitzpatrick, J. O'Sullivan and H. M. Snow

The effects of changes in the mean (S_m) and pulsatile (S_p) components of arterial wall shear stress on arterial dilatation of the iliac artery of the anaesthetized dog were examined in the absence and presence of the endothelin receptor antagonist tezosentan (10 mg kg^-1 I.V.; Ro 61-0612; [5-isopropyl-pyridine-2-sulphonic acid 6-(2-hydroxy-ethoxy)-5-(2-methoxy-phenoxy)-2-(2-1H-tetrazol-5-yl-pyridin-4-yl)-pyrimidin-4-ylamide]). Changes in shear stress were brought about by varying local peripheral resistance and stroke volume using a distal infusion of acetylcholine and stimulation of the left ansa subclavia. An increase in S_m from 1.81 ± 0.3 to 7.29 ± 0.7 N m^-2 (means ± S.E.M.) before tezosentan caused an endothelium-dependent arterial dilatation which was unaffected by administration of tezosentan for a similar increase in S_m from 1.34 ± 0.6 to 5.76 ± 1.4 N m^-2 (means ± S.E.M.). In contrast, increasing the S_p from 7.1 ± 0.8 to a maximum of 11.5 ± 1.1 N m^-2 (means ± S.E.M.) before tezosentan reduced arterial diameter significantly. Importantly, after administration of tezosentan subsequent increases in S_p caused arterial dilatation for the same increase in S_p achieved prior to tezosentan, increasing from a baseline of 4.23 ± 0.4 to a maximum of 9.03 ± 0.9 N m^-2 (means ± S.E.M.; P < 0.001). In conclusion, the results of this study provide the first in vivo evidence that pulsatile shear stress is a stimulus for the release of endothelin from the vascular endothelium.

This article has been cited by other articles:

				R. F. Kelly and H. M. Snow Characteristics of the response of the iliac artery to wall shear stress in the anaesthetized pig J. Physiol., July 15, 2007; 582(2): 731 - 743. [Abstract] [Full Text] [PDF]

				R. D. Shipley, S. J. Kim, and J. M. Muller-Delp Time course of flow-induced vasodilation in skeletal muscle: contributions of dilator and constrictor mechanisms Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1499 - H1507. [Abstract] [Full Text] [PDF]

				C. E. Hall, R. Hurtado, K. W. Hewett, M. Shulimovich, C. P. Poma, M. Reckova, C. Justus, D. J. Pennisi, K. Tobita, D. Sedmera, et al. Hemodynamic-dependent patterning of endothelin converting enzyme 1 expression and differentiation of impulse-conducting Purkinje fibers in the embryonic heart Development, February 1, 2004; 131(3): 581 - 592. [Abstract] [Full Text] [PDF]

				M. Reckova, C. Rosengarten, A. deAlmeida, C. P. Stanley, A. Wessels, R. G. Gourdie, R. P. Thompson, and D. Sedmera Hemodynamics Is a Key Epigenetic Factor in Development of the Cardiac Conduction System Circ. Res., July 11, 2003; 93(1): 77 - 85. [Abstract] [Full Text] [PDF]