Table 3.

Involvement of A₁AR and A_2AAR on L-arginine transport in HUVECs

	V max (pmol/μg protein/min)	K m (μM)	V max/K m (pmol/μg protein/min/(μM))
Normal pregnancies
Without insulin
Control	1.3 ± 0.3	91 ± 18	0.0142 ± 0.0030
KDA1AR	1.1 ± 0.3	99 ± 19	0.0111 ± 0.0026
KDA2AAR	1.1 ± 0.2	97 ± 32	0.0113 ± 0.0028
With insulin
Control	2.6 ± 0.2*	99 ± 24	0.0263 ± 0.0042*
KDA1AR	2.5 ± 0.3*	92 ± 22	0.0272 ± 0.0049*
KDA2AAR	1.2 ± 0.2†	89 ± 27	0.0135 ± 0.0032†
GDM pregnancies
Without insulin
Control	3.9 ± 0.4*	97 ± 25	0.0402 ± 0.0053*
KDA1AR	3.4 ± 0.3*	93 ± 23	0.0366 ± 0.0083*
KDA2AAR	1.4 ± 0.4†	87 ± 35	0.0161 ± 0.0090†
With insulin
Control	1.5 ± 0.4	88 ± 29	0.0170 ± 0.0051
KDA1AR	4.2 ± 0.6*†‡	83 ± 27	0.0506 ± 0.0118*†‡
KDA2AAR	1.1 ± 0.3	97 ± 26	0.0113 ± 0.0031

Data are presented as mean ± SEM (n = 29). L-Arginine transport (0–1000 μM, 1 min, 37 °C) was measured in HUVECs from normal (Normal pregnancies) or gestational diabetes mellitus (GDM pregnancies) pregnancies exposed (8 h) to culture medium without (Without insulin) or with (With insulin) insulin (1 nM). Transport assays were done in cells expressing A₁AR and A_2AAR (Control), cells knockdown for A₁AR (^KDA₁AR) or for A_2AAR (^KDA_2AAR) as described in “Materials and methods.” Maximal velocity (V _max) and apparent Michaelis-Menten constant (K _m) of saturable transport were calculated assuming a single Michaelis-Menten hyperbola. V _max/K _m represents maximal L-arginine transport capacity

*P < 0.05 versus corresponding values in Normal pregnancies Without insulin; †P < 0.05 versus corresponding Control; ‡P < 0.03 versus corresponding values in ^KDA_2AAR