Visceral periadventitial adipose tissue regulates arterial tone of mesenteric arteries.
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+ (K(v)) channels with 4-aminopyridine (2 mmol/L) or 3,4-diaminopyridine (1 mmol/L). Blocking other K+ channels with glibenclamide (3 micromol/L), apamin (1 micromol/L), iberiotoxin (100 nmol/L), tetraethylammonium ions (1 mmol/L), tetrapentylammonium ions (10 micromol/L), or Ba2+ (3 micromol/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 K(v) channel activation in vascular smooth muscle cells.
Franz Volhard Clinic and Max Delbrück Center for Molecular Medicine, Charité University Hospitals, Humboldt University of Berlin, HELIOS Klinikum Berlin, Germany.
Stefan
S
Verlohren
Galyna
G
Dubrovska
Suk-Ying
SY
Tsang
Kirill
K
Essin
Friedrich C
FC
Luft
Yu
Y
Huang
Maik
M
Gollasch
D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / Q000494:pharmacology; D015761:4-Aminopyridine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000273:Adipose Tissue / Q000378:metabolism / Q000502:physiology*; D000077770:Amifampridine; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001464:Barium / Q000494:pharmacology; D019806:Cromakalim / Q000494:pharmacology; D051668:Delayed Rectifier Potassium Channels; D019332:Endothelin-1 / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D008297:Male; D017538:Mesenteric Artery, Superior / Q000187:drug effects / Q000502:physiology*; D010455:Peptides / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects / Q000502:physiology*; D000644:Quaternary Ammonium Compounds / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology; D014655:Vascular Resistance / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014781:Viscera
D051668:Delayed Rectifier Potassium Channels; D019332:Endothelin-1; D010455:Peptides; D026902:Potassium Channel Blockers; D024642:Potassium Channels, Voltage-Gated; D000644:Quaternary Ammonium Compounds; D019806:Cromakalim; D010656:Phenylephrine; D001030:Apamin; D001464:Barium; D012701:Serotonin; D019789:Tetraethylammonium; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; C064719:iberiotoxin; C027435:tetrapentylammonium; D015761:4-Aminopyridine; D000077770:Amifampridine; D011188:Potassium; D005905:Glyburide