This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Boulanger, C. M. Articles by Vanhoutte, P. M. Search for Related Content PubMed PubMed Citation Articles by Boulanger, C. M. Articles by Vanhoutte, P. M.

Hypertension, Vol 21, 289-293, Copyright © 1993 by American Heart Association

ARTICLES

Interleukin-2 causes endothelium-dependent contractions to arachidonic acid

CM Boulanger and PM Vanhoutte
Department of Medicine-Hypertension, Baylor College of Medicine, Houston, Tex. 77030.

The present experiments were designed to investigate the effect of interleukin-2 on the response to arachidonic acid in rings with and without endothelium from Wistar-Kyoto (WKY) and spontaneously hypertensive rat (SHR) aortas. In control rings, arachidonic acid induced contractions of WKY aorta that were not different between preparations with and without endothelium. Incubation with interleukin- 2 (10 units/mL) for 6 or 18 hours augmented the response to arachidonic acid in rings with, but not in those without, endothelium from WKY rat aortas. In the WKY aorta, both the endothelium-dependent and endothelium-independent contractions to arachidonic acid observed after incubation with interleukin-2 were abolished by indomethacin and ridogrel (a thromboxane-endoperoxide receptor antagonist and a thromboxane synthase inhibitor) but were not affected by dazoxiben (a thromboxane synthase inhibitor). Interleukin-2 did not augment the vascular reactivity of WKY aortic smooth muscle to activation of the thromboxane-endoperoxide receptor with U46619. In aortas from SHRs, arachidonic acid evoked endothelium-dependent contraction; interleukin- 2 did not modify the response to arachidonic acid in preparations with and without endothelium. These data demonstrate that 1) endothelium- dependent contractions to arachidonic acid are observed in SHR but not in WKY rat aortas; 2) interleukin-2 induces endothelium-dependent contractions to arachidonic acid in the WKY aorta that are mediated by an augmented release of a metabolite of cyclooxygenase, different from thromboxane A2 but activating thromboxane-endoperoxide receptors; and 3) interleukin-2 does not affect the endothelium-dependent and endothelium-independent response to arachidonic acid in the SHR aorta.

This article has been cited by other articles:

				A Belda, J Borras-Blasco, L Lopez-Montes, D Rosique-Robles, E Castera, and J Abad Foot ischaemia and toe skin necrosis associated with interleukin-2 infusion in an HIV-infected patient Int J STD AIDS, August 1, 2009; 20(8): 577 - 579. [Abstract] [Full Text] [PDF]

				E. H. C. Tang, M. Feletou, Y. Huang, R. Y. K. Man, and P. M. Vanhoutte Acetylcholine and sodium nitroprusside cause long-term inhibition of EDCF-mediated contractions Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2434 - H2440. [Abstract] [Full Text] [PDF]

				A. Dellipizzi, M. L. Pucci, A. Y. Mosny, K. Deseyn, and A. Nasjletti Contribution of Constrictor Prostanoids to the Calcium-Dependent Basal Tone in the Aorta from Rats with Aortic Coarctation-Induced Hypertension: Relationship to Nitric Oxide J. Pharmacol. Exp. Ther., October 1, 1997; 283(1): 75 - 81. [Abstract] [Full Text]