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 (KATP 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 (KV channel blocker) equally 
increased fetoplacental arterial pressure in controls, and in diabetes (21 +/- 4 
mm Hg vs 22 +/- 2 mm Hg). Apamin and charybdotoxin (KCa channel blockers) caused 
a negligible rise in fetoplacental arterial pressure.
CONCLUSION: In the fetoplacental circulation, KATP channels and KV channels 
significantly contribute to baseline vascular tone. In diabetes, vascular KATP 
channel function is impaired.