Differential effect of nicotine on intracellular calcium concentration ([Ca2+]i) in human umbilical artery and vein endothelial cells

Abstract

Maternal tobacco smoke (TS) exposure is associated with intrauterine growth retardation and low birth weight, both of which increase infant morbidity and mortality. Nicotine, an active component in TS, also decreases birth weight and postnatal weight gain, although the mechanisms involved remain unclear. We hypothesized that in umbilical endothelial cells (ECs), nicotine alters regulation of [Ca2+]i, an important modulator of synthesis and release of endothelial‐derived vasoactive factors and, consequently, umbilical vessel tone and blood flow to and from the fetus. In this study, we used fluorescent microscopy in human umbilical artery ECs (HUAECs) and human umbilical vein ECs (HUVECs) loaded with the Ca2+‐sensitive dye, Fura‐2. In HUAECs, we found that acute (10 min) application of nicotine (100 ng/ml) caused an immediate decrease in [Ca2+]i. Prolonged nicotine treatment (10 or 100 ng/ml; 24 hr) also decreased resting [Ca2+]i. In contrast, both acute (100 ng/ml; 10 min) and prolonged (10 or 100 ng/ml; 24 hr) exposure to nicotine increased [Ca2+]i in HUVECs. Our results indicate that nicotine, at concentrations comparable to plasma levels in smokers and non‐smokers exposed to environmental TS, caused both acute and long‐lasting alterations in [Ca2+]i in HUAECs and HUVECs and suggest that nicotine may differentially regulate vasoactive factor synthesis and vascular tone in umbilical arteries and veins.