Journal article
Dilatation of cerebral arterioles in response to activation of adenylate cyclase is dependent on activation of Ca2+-dependent K+ channels
Circulation research, Vol.76(6), pp.1057-1062
1995
DOI: 10.1161/01.RES.76.6.1057
PMID: 7758160
Abstract
The role of Ca(2+)-dependent potassium channels in mediating vascular responses to activation of adenylate cyclase in vivo is not known. The goal of this study was to examine the hypothesis that dilatation of cerebral arterioles in response to activation of adenylate cyclase is mediated by activation of Ca(2+)-dependent potassium channels. Diameters of cerebral arterioles were measured in vivo in anesthetized rabbits. Topical application of forskolin (1 and 10 mumol/L), a direct activator of adenylate cyclase, dilated cerebral arterioles by 40 +/- 8% (mean +/- SEM) and 71 +/- 9%, respectively, from a control diameter of 85 +/- 4 microns. Iberiotoxin (50 and 100 nmol/L), a selective inhibitor of Ca(2+)-dependent potassium channels, inhibited dilatation in response to both concentrations of forskolin by 45% to 60%. We obtained similar results by using charybdotoxin (50 nmol/L), another inhibitor of Ca(2+)-dependent potassium channels. Vasodilatation in response to dibutyryl cAMP (a cell-permeable cAMP analogue) was also inhibited by iberiotoxin. In contrast, dilatation of cerebral arterioles in response to sodium nitroprusside and acetylcholine (activators of guanylate cyclase) and aprikalim (activator of ATP-sensitive potassium channels) was not inhibited by iberiotoxin. These findings suggest that dilatation of cerebral arterioles in response to forskolin and increases in intracellular concentrations of cAMP are mediated by activation of Ca(2+)-dependent potassium channels. Thus, activation of Ca(2+)-dependent potassium channels may be a major mechanism of cerebral vasodilatation in response to activation of adenylate cyclase in vivo.
Details
- Title: Subtitle
- Dilatation of cerebral arterioles in response to activation of adenylate cyclase is dependent on activation of Ca2+-dependent K+ channels
- Creators
- H TAGUCHI - Univ. Iowa coll. medicine, cardiovascular cent. and cent. aging, Iowa City IA 52242, United StatesD. D HEISTAD - Univ. Iowa coll. medicine, cardiovascular cent. and cent. aging, Iowa City IA 52242, United StatesT KITAZONO - Univ. Iowa coll. medicine, cardiovascular cent. and cent. aging, Iowa City IA 52242, United StatesF. M FARACI - Univ. Iowa coll. medicine, cardiovascular cent. and cent. aging, Iowa City IA 52242, United States
- Resource Type
- Journal article
- Publication Details
- Circulation research, Vol.76(6), pp.1057-1062
- Publisher
- Lippincott; Hagerstown, MD
- DOI
- 10.1161/01.RES.76.6.1057
- PMID
- 7758160
- ISSN
- 0009-7330
- eISSN
- 1524-4571
- Language
- English
- Date published
- 1995
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040496002771
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