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Am J Physiol Regul Integr Comp Physiol 266: R1148-R1153, 1994;
0363-6119/94 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 4 1148-R1153, Copyright © 1994 by American Physiological Society

ARTICLES

Cardiovascular effects of human recombinant interleukin-1 beta in conscious rats

A. Bataillard and J. Sassard
Department of Physiology and Clinical Pharmacology, Faculty of Pharmacy, Centre National de la Recherche Scientifique Unite de Recherche Associee 1483, Lyon, France.

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.


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