In vivo properties of potassium channels in cerebral blood vessels during diabetes mellitus

William G. Mayhan, Jill F. Mayhan, Hong Sun, Kaushik P. Patel

Research output: Contribution to journalArticle

23 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)605-613
Number of pages9
JournalMicrocirculation
Volume11
Issue number7
DOIs
StatePublished - Oct 1 2004

Fingerprint

Potassium Channels
Blood Vessels
Diabetes Mellitus
Arterioles
Basilar Artery
Dilatation
4-Aminopyridine
Tetraethylammonium
Vasoconstriction
Calcium-Activated Potassium Channels
Vasodilation
barium chloride

Keywords

  • 4-AP
  • BaCl
  • Basilar artery
  • Brain
  • Diabetes
  • KCl
  • NS-1619
  • Pial arterioles
  • Potassium channels
  • Stroke
  • TEA

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

In vivo properties of potassium channels in cerebral blood vessels during diabetes mellitus. / Mayhan, William G.; Mayhan, Jill F.; Sun, Hong; Patel, Kaushik P.

In: Microcirculation, Vol. 11, No. 7, 01.10.2004, p. 605-613.

Research output: Contribution to journalArticle

@article{8b48240d245946319c5b311470190700,
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.",
keywords = "4-AP, BaCl, Basilar artery, Brain, Diabetes, KCl, NS-1619, Pial arterioles, Potassium channels, Stroke, TEA",
author = "Mayhan, {William G.} and Mayhan, {Jill F.} and Hong Sun and Patel, {Kaushik P.}",
year = "2004",
month = "10",
day = "1",
doi = "10.1080/10739680490503410",
language = "English (US)",
volume = "11",
pages = "605--613",
journal = "Microcirculation",
issn = "1073-9688",
publisher = "Wiley-Blackwell",
number = "7",

}

TY - JOUR

T1 - In vivo properties of potassium channels in cerebral blood vessels during diabetes mellitus

AU - Mayhan, William G.

AU - Mayhan, Jill F.

AU - Sun, Hong

AU - Patel, Kaushik P.

PY - 2004/10/1

Y1 - 2004/10/1

N2 - 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.

AB - 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.

KW - 4-AP

KW - BaCl

KW - Basilar artery

KW - Brain

KW - Diabetes

KW - KCl

KW - NS-1619

KW - Pial arterioles

KW - Potassium channels

KW - Stroke

KW - TEA

UR - http://www.scopus.com/inward/record.url?scp=10244219782&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=10244219782&partnerID=8YFLogxK

U2 - 10.1080/10739680490503410

DO - 10.1080/10739680490503410

M3 - Article

C2 - 15513870

AN - SCOPUS:10244219782

VL - 11

SP - 605

EP - 613

JO - Microcirculation

JF - Microcirculation

SN - 1073-9688

IS - 7

ER -