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Emerging Concepts in Ion Channel Biophysics
Poster Abstracts
50
34-POS
Board 34
Role of Calcium-activated Potassium Channels in L-arginine/NO Pathway Regulation by
Insulin in Human Fetal Endothelium.
Emerita Basualto
1
, Susana Rojas
1
, Marcela Cid
3
,
Marcelo Gonzalez
1,2
.
1
University of Concepcion, Concepción, Chile,
2
Group of Research and Innovation in Vascular
Health (GRIVAS Health), Chillan, Chile,
3
University of Concepcion, Concepcion, Chile.
The regulation of vascular tone of placenta is a key mechanism for an adequate nutrition of the
fetus and this mechanism is regulated by paracrine and endocrine signals. Between these signals,
insulin is an hormone that have a important role, especially when the fetus develops his pancreas,
acting directly on endothelial cells of umbilical cord and placenta. A main mechanism for
regulation of vascular tone is related with the endothelial activity of calcium-activated potassium
channels (KCa). In this study we want to determine if the mechanism of relaxation induced by
insulin is dependent of KCa channels. Placenta and umbilical cords were obtained from normal
pregnancies for placental vascular reactivity assays and isolation of human umbilical vein
endothelial cells (HUVEC). Isometric tension and placental pressure were determined through
wire myogaphy and isolated cotyledon perfusion, respectively, in vessels incubated with insulin
and/or tetra ethyl ammonium (TEA, K
+
channels inhibitor), iberiotoxin (BKCa ihibitor) and
Tram-34 (SKCa inhibitor). In HUVEC, after similar treatment, the plasma membrane polarity
changes (with DiBAC4(3) dye), nitric oxide synthesis (with DAF) and L-arginine transport were
determined. Insulin induces relaxation in placental vein and lower perfusion pressure in placenta,
both effects were blocked with KCa channels inhibitors. In HUVEC, the stimulation of insulin
on NO synthesis and L-arginine transport were decreased with iberiotoxin and Tram-34. In
plasma membrane polarity, the co-incubation with insulin prevent the depolarization induced by
Tram-34 and iberiotoxin. The vasodilatation induced by insulin is a mechanism that depends on
L-arginine transport and NO synthesis. Our results showed that this mechanism could require a
previous step of plasma membrane hyperpolarization induced by activation of BKCa or SKCa in
human fetal endothelium. Supported by VRID-Enlace 216.033.108-1.0 and VRID-Asociativo
213.A84.014-1.0, Universidad de Concepción, Chile.