gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Adiponectin is a novel potent vasodilator

Meeting Abstract

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  • G. Fésüs - Franz-Volhard-Klinik, Charité Universitätsmedizin Berlin Campus Buch (Berlin, D)
  • F.C. Luft - Franz-Volhard-Klinik, Charité Universitätsmedizin Berlin Campus Buch (Berlin, D)
  • M. Gollasch - Campus Virchow-Klinikum (Berlin, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP5

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/hoch2005/05hoch005.shtml

Published: August 8, 2006

© 2006 Fésüs et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Small mesenteric arteries are surrounded by adipose tissue, which produces a number of biologically active substances including adiponectin. Perivascular adipose tissue secretes adipocyte-derived relaxing factor (ADRF) to relax mesenteric arteries by opening of smooth muscle delayed-rectifier K+ (Kv) channels in rats. The nature of ADRF is unknown. We studied adiponectin gene-deficient mice and tested the hypotheses that adiponectin represents a potent humoral vasodilator and plays a role in the paracrine control of mesenteric vascular tone by perivascular adipose tissue. In isolated mouse mesenteric arteries, recombinant adiponectin (5 µg/ml) inhibited serotonin-dependent contractions. The effects were reduced by inhibition of Kv channels with 4-aminopyridine (4-AP, 2 mM). The contractile response to serotonin was markedly reduced in intact vessels compared to vessels without perivascular fat. To study vascular function in adiponectin-deficient mice, the mesenteric bed (MB) was cannulated and perfused at a constant flow of 4-5 mL/min in the absence and presence of serotonin. Inhibition of Kv channels with 4-AP (2 mmol/L) induced a similar increase in perfusion pressure in MB of adiponectin-deficient mice, compared to wild-type mice. The anti-contractile effects of perivascular fat were similar in mesenteric artery and aortic rings from adiponectin-deficient mice and wild-type mice. Our data indicate that adiponectin functions as a novel potent vasodilator, which relaxes mesenteric rings by opening Kv channels. However, adiponectin does not play a role in the paracrine control of vascular tone by perivascular adipose tissue in this vascular bed.