Journal article
Responses of cerebral arterioles in diabetic rats to activation of ATP-sensitive potassium channels
American journal of physiology. Heart and circulatory physiology, Vol.265(1), pp.H152-H157
07/01/1993
DOI: 10.1152/ajpheart.1993.265.1.H152
PMID: 8342628
Abstract
The goal of this study was to determine whether responses of pial arterioles to activation of ATP-sensitive potassium channels are altered during diabetes mellitus. We measured changes in diameter of pial arterioles in vivo in nondiabetic and diabetic rats (streptozotocin; 50–60 mg/kg ip; studied 3–4 mo after streptozotocin) in response to RP52891, an activator of ATP-sensitive potassium channels. RP52891 (1.0 microM) dilated pial arterioles in nondiabetic rats by 16 +/- 1% but constricted pial arterioles in diabetic rats by 2 +/- 2% (means +/- SE; P < 0.05 vs. response in nondiabetic rats). Dilatation of pial arterioles in nondiabetic rats in response to RP52891 was inhibited by glibenclamide (1.0 microM) but was not altered by NG-monomethyl-L-arginine (1.0 microM), apamin (0.1 microM), or charybdotoxin (50 nM). Thus dilatation of pial arterioles in response to RP52891 appears to be due to activation of ATP-sensitive potassium channels and does not involve nitric oxide or calcium-activated potassium channels. To determine whether impaired dilatation of pial arterioles in response to RP52891 in diabetic rats was related to a nonspecific effect of diabetes mellitus on vasodilatation, we measured diameter of pial arterioles in nondiabetic and diabetic rats in response to nitroglycerin. Nitroglycerin (1.0 microM) dilated pial arterioles by 12 +/- 1% in nondiabetic rats and 16 +/- 2% in diabetic rats (P > 0.05). Thus impaired dilatation of pial arterioles in diabetic rats in response to RP52891 also is not related to a nonspecific effect of diabetes mellitus on vasodilatation.
Details
- Title: Subtitle
- Responses of cerebral arterioles in diabetic rats to activation of ATP-sensitive potassium channels
- Creators
- William G Mayhan - Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha 68198Frank M Faraci - Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha 68198
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.265(1), pp.H152-H157
- DOI
- 10.1152/ajpheart.1993.265.1.H152
- PMID
- 8342628
- NLM abbreviation
- Am J Physiol Heart Circ Physiol
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 07/01/1993
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040366602771
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