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Articles in PresS, published online ahead of print April 11, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00544.2001
Submitted on September 6, 2001
Accepted on April 4, 2002
1 Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
* To whom correspondence should be addressed. E-mail: Ping.Wang{at}ccc.uab.edu.
Adrenomedullin (AM), a potent vasodilatory peptide, plays an important role in initiating the hyperdynamic response during the early stage of sepsis. Moreover, the reduced vascular responsiveness to AM appears to be responsible for the transition from the early, hyperdynamic phase to the late, hypodynamic phase of sepsis. Although the novel specific AM binding protein-1 (AMBP-1) enhances AM-mediated action in a cultured cell line, it remains to be determined whether AMBP-1 plays any role in modulating vascular responsiveness to AM during sepsis. To study this, adult male rats were subjected to sepsis by cecal ligation and puncture (CLP). The thoracic aorta was harvested for determining AM-induced vascular relaxation. Aortic levels of AMBP-1 were determined by Western blot analysis and AM receptor gene expression in the aortic tissue was assessed by RT-PCR. The results indicate AMBP-1 significantly enhanced AM-induced vascular relaxation in aortic rings from sham-operated animals. Although vascular responsiveness to AM decreased at 20 h after CLP (i.e., the late, hypodynamic stage of sepsis), addition of AMBP-1 in vitro restored the vascular relaxation induced by AM. Moreover, the aortic level of AMBP-1 decreased significantly at 20 h after CLP. In contrast, AM receptor gene expression was not altered under such conditions. These results, taken together, suggest that AMBP-1 plays an important role in modulating vascular responsiveness to AM, and the reduced AMBP-1 appears to be responsible for the vascular AM hyporesponsiveness observed during the hypodynamic phase of sepsis.
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