Impaired K_ATP channel function in the fetoplacental circulation of patients with type 1 diabetes mellitus

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• 作者：Tanya M. Bisseling ; Marieke G. Versteegen ; Selina van der Wal ; Jenny J.H. Copius Peereboom-Stegeman ; Joop M.P.M. Borggreven ; Eric A.P. Steegers ; Jeroen A.W.M. van der Laak ; Frans G.M. Russel ; Paul Sm
• 关键词：Diabetes ; Potassium channel ; Glibenclamide ; Fetoplacental vasculature ; Endothelium ; Pregnancy
• 刊名：American Journal of Obstetrics and Gynecology
• 出版年：2005
• 出版时间：March 2005
• 年：2005
• 卷：192
• 期：3
• 页码：973-979
• 全文大小：197 K

文摘

Objective

The increased perinatal morbidity in diabetes may be partly related to vascular dysfunction. Because potassium channels play an important role in the regulation of vascular tone, this study explores the impact of diabetes on potassium channel function in the fetoplacental vascular bed.

Study design

Vascular potassium channel function was investigated by ex vivo dual perfusion of isolated placental cotyledons (n = 47). Appropriate control experiments were carried out to exclude nonspecific effects.

Results

Glibenclamide (K_ATP channel blocker) increased perfusion pressure to a maximum fetoplacental arterial pressure of 37 ± 6 mm Hg in controls versus 15 ± 6 mm Hg in diabetes (P < .05). 4-Aminopyridine (K_V channel blocker) equally increased fetoplacental arterial pressure in controls, and in diabetes (21 ± 4 mm Hg vs 22 ± 2 mm Hg). Apamin and charybdotoxin (K_Ca channel blockers) caused a negligible rise in fetoplacental arterial pressure.

Conclusion

In the fetoplacental circulation, K_ATP channels and K_V channels significantly contribute to baseline vascular tone. In diabetes, vascular K_ATP channel function is impaired.