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Abnormal diazoxide induced vasodilation in cerebral arteries from Zucker obese rats with insulin resistance
Author(s) -
Katakam Prasad V.G,
Snipes James A,
Busija Anna,
Busija David W
Publication year - 2007
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.21.6.a1262-c
Subject(s) - vasodilation , diazoxide , endocrinology , medicine , chemistry , iberiotoxin , activator (genetics) , insulin , receptor
Diazoxide (DZ), a mitochondrial K ATP channel activator elicits arterial vasodilation by increasing the generation of mitochondria‐derived reactive oxygen species (ROS) that stimulate Ca 2+ sparks and Ca 2+ activated K + channels. We evaluated the DZ induced vasodilation in isolated cerebral arteries from Zucker obese (ZO) and lean (ZL) rats by videomicroscopy. DZ induced vasodilation was diminished in ZO compared to ZL. 3‐nitropropionic acid, an activator of mitochondrial ROS generation, has no affect on vasodilation in ZL, but enhances DZ induced vasodilation in ZO. DZ induced vasodilation was partially inhibited by iberiotoxin in ZL while it was totally abolished in ZO. ZO arteries exhibit reduced pressure induced constriction compared to ZL. However, vasodilation to nitroprusside was similar in both ZO and ZL. Thus, cerebral arteries from ZO exhibit abnormal DZ induced vasodilation mediated by reduced generation of mitochondrial ROS and/or Ca 2+ sparks.