Although obesity increases the risk for hypertension in pregnancy, the mechanisms responsible are unknown. Increased nitric oxide (NO) production results in vasodilation and reduced blood pressure during normal pregnancy in lean rats; however, the role of NO is less clear during obese pregnancies. We examined the impact of obesity on NO synthase (NOS)-mediated regulation of blood pressure during pregnancy by testing the hypothesis that NOS activity, expression and regulation of vascular tone and blood pressure are reduced in obese pregnant rats. At gestational day 19, melanocortin-4 receptor (MC4R)-deficient obese rats (MC4R^+/-) had greater body weight and fat mass with elevated blood pressure and circulating sFlt-1 levels compared to MC4R^+/+ pregnant rats. MC4R^+/- pregnant rats also had less circulating cGMP levels and reduced total NOS enzymatic activity and expression in mesenteric arteries. Despite decreased biochemical measures of NO/NOS in MC4R^+/- rats, NOS inhibition enhanced vasoconstriction only in mesenteric arteries from MC4R^+/- rats, suggesting greater NOS-mediated tone. To examine the role of NOS on blood pressure regulation in obese pregnant rats, MC4R^+/- and MC4R^+/+ pregnant rats were administered the non-selective NOS inhibitor L-NG-Nitroarginine methyl ester (L-NAME, 100 mg/L) from gestational day 14 to 19 in drinking water. The degree by which L-NAME raised blood pressure was similar between obese and lean pregnant rats. Although MC4R^+/- obese pregnant rats had elevated blood pressure associated with reduced total NOS activity and expression, they had enhanced NOS-mediated attenuation of vasoconstriction, with no evidence of alterations in NOS-mediated regulation of blood pressure.