title: In vivo properties of potassium channels in cerebral blood vessels during diabetes mellitus.
abstract: OBJECTIVE
  While potassium (K+) channels are important in basal tone and dilatation of large and small cerebral vessels, the effect of diabetes mellitus on K+ channels remains unclear. The goal of this study was to identify the influence of diabetes on responses of cerebral vessels to inhibition/activation of K+ channels.
  
  
  METHODS
  The authors measured in vivo responses of pial arterioles and the basilar artery to inhibition/activation of K+ channels in nondiabetic and diabetic rats using intravital microscopy.
  
  
  RESULTS
  Pial arterioles from nondiabetic and diabetic rats constricted to barium chloride (BaCl2) and 4-aminopyridine (4-AP). However, the magnitude of vasoconstriction to BaCl2 was greater in nondiabetic than in diabetic rats. Tetraethylammonium (TEA) did not alter diameter of pial arterioles in nondiabetic or diabetic rats. In addition, dilatation of pial arterioles to KCl and NS-1619 was less in diabetic compared to nondiabetic rats. The basilar artery from nondiabetic and diabetic rats constricted in a similar manner to BaCl2 and 4-AP. In contrast, vasoconstriction to TEA was greater in diabetic than nondiabetic rats. Similar to that reported for pial arterioles, dilatation of the basilar artery to KCl and NS-1619 was less in diabetic than nondiabetic rats.
  
  
  CONCLUSIONS
  Inward-rectifier (Kir) and voltage-dependent (Kv), but not calcium-activated (Kca), K+ channels are active under basal conditions in pial arterioles, while Kir, Kv, and Kca are active under basal conditions in the basilar artery of nondiabetic and diabetic rats. In addition, activation of Kir and Kca channels produces less cerebral vasodilatation in diabetic compared to nondiabetic rats. These findings provide new and important information regarding the influence of diabetes on the role of K+ channels in the regulation of cerebral vascular diameter.
authors.affiliation: Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA. wgmayhan@unmc.edu
authors.forename: William G
authors.initials: WG
authors.lastname: Mayhan
authors.forename: Jill F
authors.initials: JF
authors.lastname: Mayhan
authors.forename: Hong
authors.initials: H
authors.lastname: Sun
authors.forename: Kaushik P
authors.initials: KP
authors.lastname: Patel
mesh_terms: D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000503:physiopathology; D017609:Barium Compounds; D001488:Basilar Artery / Q000187:drug effects / Q000503:physiopathology; D001562:Benzimidazoles / Q000494:pharmacology; D001921:Brain / Q000098:blood supply* / Q000378:metabolism*; D002712:Chlorides; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D010841:Pia Mater / Q000098:blood supply / Q000378:metabolism; D015221:Potassium Channels / Q000145:classification / Q000187:drug effects / Q000378:metabolism*; D024681:Potassium Channels, Calcium-Activated / Q000187:drug effects / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects / Q000378:metabolism; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects / Q000378:metabolism; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D017609:Barium Compounds; D001562:Benzimidazoles; D002712:Chlorides; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; D024661:Potassium Channels, Inwardly Rectifying; D024642:Potassium Channels, Voltage-Gated; C024986:barium chloride; C086491:NS 1619; D011189:Potassium Chloride