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Am J Physiol Regul Integr Comp Physiol (November 29, 2001). doi:10.1152/ajpregu.00520.2001
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Articles in PresS, published online ahead of print November 29, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00520.2001
Submitted on August 30, 2001
Accepted on November 24, 2001

Cytokine-mediated downregulation of vasopressin V1A-receptors during acute endotoxemia in rats

Michael Bucher1*, Jonny Hobbhahn1, Kai Taeger1, and Armin Kurtz2

1 Department of Anesthesiology, University of Regensburg, Regensburg, Germany
2 Department of Physiology, University of Regensburg, Regensburg, Germany

* To whom correspondence should be addressed. E-mail: michael.bucher{at}klinik.uni-regensburg.de.

The reduced pressure response to vasopressin during acute sepsis has directed our interest onto the regulation of vasopressin V1A-receptors. Rats were injected with lipopolysaccharide for induction of experimental Gram-negative sepsis. V1A-receptor gene expression was downregulated in the liver, lung, kidney and heart during endotoxemia. As the concentrations of proinflammatory cytokines such as IL-1ß, TNF-{alpha} and IFN-{gamma} were highly increased during sepsis the influence of these cytokines on V1A-receptor expression was investigated in primary cultures of hepatocytes and in the aortic vascular smooth muscle cell line A7r5. It turned out that V1A-receptor expression was downregulated by the cytokines in a nitric oxide-independent manner. Blood pressure dose-response studies after injection of endotoxin showed a diminished responsiveness to the selective V1-receptor agonist Phe2, Ile3, Orn8-vasopressin. Our data show that sepsis causes a downregulation of V1A-receptors, and suggest that this effect is likely mediated by proinflammatory cytokines. We propose that this downregulation of V1A-receptors contributes to the attenuated responsiveness of blood pressure in response to vasopressin, and therefore contributes to the circulatory failure in septic shock.




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