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Activation of endothelial Ca2+‐activated potassium channels can improve endothelial function in basilar arteries from diabetic rats
Author(s) -
Plane Frances,
Walsh Emma,
Cole William C
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1231
Subject(s) - basilar artery , medicine , endocrinology , vasodilation , endothelium , acetylcholine , nitric oxide , chemistry , endothelial dysfunction
Endothelium‐dependent relaxation of isolated rat basilar artery to acetylcholine (ACh) can be fully accounted for by the release of endothelium‐derived NO. In addition, activation of endothelial Ca 2+ ‐activated potassium channels (K Ca ) plays a key role in modulating ACh‐stimulated production of endothelium‐derived nitric oxide (NO) in this artery. Thus, we have investigated whether activation of endothelial small (SK Ca ) and intermediate (IK Ca ) K Ca by 1‐ethyl‐2‐benzimidazolinone (1‐EBIO) can improve endothelial function in basilar arteries from diabetic rats. Relaxations to ACh (0.01–30 μM) were significantly depressed in isolated basilar arteries from Streptozotocin‐treated (STZ) diabetic rats compared to vessels from control animals. In contrast, relaxation of basilar arteries evoked by 1‐EBIO (1–300 μM), was not significantly different in arteries from STZ and control rats. Application of low concentrations of 1‐EBIO (1–5 μM) significantly enhanced ACh‐evoked relaxations in basilar arteries from STZ‐treated rats. Pre‐incubation with L‐NAME abolished relaxations to ACh both in the presence and absence of 1‐EBIO indicating that the enhancement of ACh‐evoked responses was due to increased production of NO. Quantitative real‐time PCR analysis demonstrated that mRNA levels for both SK Ca and IK Ca were not significantly different in basilar arteries from control and STZ‐treated rats. It is concluded that activation of K Ca may significantly improve endothelial function in basilar arteries from STZ‐treated diabetic rats. Supported by CIHR.