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Distinct Agonist‐Induced Contraction in Intra‐ and Extra‐Renal Arteries under High‐Glucose Conditions
Author(s) -
Nobe Koji,
Tsumita Naoki,
Nezu Yumiko,
Honda Kazuo
Publication year - 2009
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.23.1_supplement.989.8
Subject(s) - medicine , endocrinology , phenylephrine , agonist , contractility , thromboxane , thromboxane a2 , contraction (grammar) , stimulation , chemistry , renal artery , vasoconstriction , methoxamine , kidney , receptor , blood pressure , platelet
The renal artery (RA) has been extensively investigated as a model for the assessment of renal vascular function/dysfunction; however, few studies have focused on the intrarenal vasculature. We measured contractile responses in mouse interlobar artery (ILA) in this study. Treatment of RA with 10 μM phenylephrine (PE), 10 nM U46619 (thromboxane A 2 analog) or 10 μM prostaglandin F 2α elicited a response greater than 150% of the 50 mM KCl‐induced response (1698.7±323.4 μN/mm; n=5). In ILA, 10 nM U46619 produced a response that was 130% of the KCl‐induced response (784.0±56.6 µN/mm; n=5); however, other agonists induced levels similar to that of the KCl‐induced response. These results revealed that extra‐ and intrarenal arteries possess different agonist‐induced contractions. Under high‐glucose conditions (22.2 mM glucose), contractile responses in RA and ILA were enhanced significantly following PE and U46619 stimulation, respectively. Enhancement was suppressed by a calcium‐independent protein kinase C (PKC) inhibitor. Our findings suggested that only the U46619, induces enhanced contractility in ILA, which might lead to renal dysfunction and nephropathy via reduced intrarenal blood flow rate.