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Vasomotion in vivo ő the role of the endoplasmic reticulum (677.9)
Author(s) -
Aalkjaer Christian,
Nyvad Jakob,
Straarup Marthe,
Matchkov Vladimir
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.677.9
Subject(s) - vasomotion , endoplasmic reticulum , in vivo , cyclopiazonic acid , medicine , endocrinology , chemistry , mesenteric arteries , biophysics , biology , artery , vasodilation , biochemistry , microbiology and biotechnology
Low frequency high amplitude oscillation with antiphase oscillations of Ca 2+ in endothelial and smooth muscle cells are seen in rat mesenteric small arteries in vitro after inhibition of the endoplasmic reticulum (ER) Ca 2+ APTase. We here investigated the role of ER for vasomotion in vivo. Rats were anesthetized with Hypnorm/Dormicum (HD), Ketamin/Xylazin (KX) or Isofluran (ISF) and the intestine exteriorized through a laparotomy. A small mesenteric artery segment was positioned in a 100 μl reservoir and the diameter monitored. Constriction to norepinephrine (NE) was substantially reduced with HD compared to KX and ISF, and further experiments were done with KX. At intermediate NE concentrations vasomotion occurred. With cyclopiazonic acid (CPA) present frequency was reduced and amplitude increased. Inhibition of small and intermediate conductance K + channels had no effect on vasomotion without CPA, but reduced the amplitude and increased the frequency in the presence of CPA. We conclude that HD is not a suitable anesthetic for studying adrenergic mechanisms in rats, and that small and intermediate conductance K + channels are important for vasomotion in vivo, but only when the endoplasmic reticulum is inhibited.