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(Hypertension. 2004;44:271.)
© 2004 American Heart Association, Inc.
Scientific Contributions |
From the Franz Volhard Clinic and Max Delbrück Center for Molecular Medicine (S.V., G.D., K.E., F.C.L., M.G.), Charité University Hospitals, Humboldt University of Berlin, HELIOS Klinikum Berlin, Germany; Louisiana State University Health Sciences Center (M.G.), Department of Physiology, New Orleans; Department of Physiology (S.-Y.T.,Y.H.), Chinese University of Hong Kong, Shatin, China.
Correspondence to Maik Gollasch, MD, PhD, Franz Volhard Clinic, Wiltbergstraße 50, 13125 Berlin, Germany. E-mail gollasch{at}fvk-berlin.de or mgolla@lsuhsc.edu
Periadventitial adipose tissue produces vasoactive substances that influence vascular contraction. Earlier studies addressed this issue in aorta, a vessel that does not contribute to peripheral vascular resistance. We tested the hypothesis that periadventitial adipose tissue modulates contraction of smaller arteries more relevant to blood pressure regulation. We studied mesenteric artery rings surrounded by periadventitial adipose tissue from adult male Sprague-Dawley rats. The contractile response to serotonin, phenylephrine, and endothelin I was markedly reduced in intact vessels compared with vessels without periadventitial fat. The contractile response to U46619 or depolarizing high K+-containing solutions (60 mmol/L) was similar in vessels with and without periadventitial fat. The K+ channel opener cromakalim induced relaxation of vessels precontracted by serotonin but not by U46619 or high K+-containing solutions (60 mmol/L), suggesting that K+ channels are involved. The intracellular membrane potential of smooth muscle cells was more hyperpolarized in intact vessels than in vessels without periadventitial fat. Both the anticontractile effect and membrane hyperpolarization of periadventitial fat were abolished by inhibition of delayed-rectifier K+ (Kv) channels with 4-aminopyridine (2 mmol/L) or 3,4-diaminopyridine (1 mmol/L). Blocking other K+ channels with glibenclamide (3 µmol/L), apamin (1 µmol/L), iberiotoxin (100 nmol/L), tetraethylammonium ions (1 mmol/L), tetrapentylammonium ions (10 µmol/L), or Ba2+ (3 µmol/L) had no effect. Longitudinal removal of half the perivascular tissue reduced the anticontractile effect of fat by almost 50%, whereas removal of the endothelium had no effect. We suggest that visceral periadventitial adipose tissue controls mesenteric arterial tone by inducing vasorelaxation via Kv channel activation in vascular smooth muscle cells.
Key Words: muscle, smooth mesenteric arteries obesity hypertension, obesity
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