Journal article
Collateral response to activation of potassium channels in vivo
Basic research in cardiology, Vol.93(2), pp.136-142
04/1998
DOI: 10.1007/s003950050074
PMID: 9601581
Abstract
Activation of ATP-sensitive K+ channels is involved in the coronary vascular response to decreases in perfusion pressure and ischemia. Since activation of ATP-sensitive K+ channels in collateral vessels may be important in determining flow to collateral-dependent myocardium, the ability of collaterals to respond to activation of the channel was tested. In the beating heart of dogs, we compared responses of non-collaterals less than 100 microns in diameter to collaterals of similar size using computer-controlled stroboscopic epi-illumination of the left ventricle coupled to a microscope-video system. Aprikalim, a selective activator of ATP-sensitive K+ channels (0.1-10 microM) produced similar dose-dependent dilation of non-collaterals and collaterals. Relaxation was decreased by inhibition of ATP-sensitive K+ channels with glibenclamide, but not by inhibition of nitric oxide synthase with nitro-L-arginine. Bradykinin (10-100 microM) produced similar dilation of non-collaterals and collaterals which was decreased by nitro-L-arginine but not glibenclamide. Thus, in microvascular collaterals, relaxation to both nitric oxide and activation of ATP-sensitive K+ channels is similar to non-collaterals.
Details
- Title: Subtitle
- Collateral response to activation of potassium channels in vivo
- Creators
- K G Lamping - Medical Services , VA Medical Center, Iowa City 52246, USA. kathryn-lamping@uiowa.edu
- Resource Type
- Journal article
- Publication Details
- Basic research in cardiology, Vol.93(2), pp.136-142
- DOI
- 10.1007/s003950050074
- PMID
- 9601581
- ISSN
- 0300-8428
- eISSN
- 1435-1803
- Grant note
- HL 39050 / NHLBI NIH HHS
- Language
- English
- Date published
- 04/1998
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984094723602771
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