The objectives were to determine effects of 12 hourly infusions of different quantities of nicotinic acid (NA) on plasma nonesterified fatty acid (NEFA; experiment 1) and whether longer (108 h) continuous infusions of NA could induce sustained reductions of plasma NEFA (experiment 2) in nonlactating, nongestating Holstein cows that were feed restricted. Experiment 1 was a 5 × 5 Latin square with 6-d periods and 9 recovery days between each period. Each period consisted of 5 d of partial feed restriction to increase plasma NEFA concentration. Treatments were abomasal infusions of 0, 0.25, 0.5, 1, or 3 mg of NA/h per kilogram of body weight (BW), infused as hourly boluses for 12 h, starting 4 d after initiation of partial feed restriction. Plasma NEFA was decreased for the highest dose: from 448 μEq/L to 138 ± 75 μEq/L at 1 h after the first bolus of 3 mg of NA/h per kilogram of BW. This initial reduction in plasma NEFA concentration was followed by an increase in concentration at 2, 3, and 4 h relative to initiation of infusions. Plasma NEFA then decreased to 243 μEq/L 6 h after initiation of treatments and remained low until termination of infusions. A rebound in plasma NEFA concentration occurred at 3 and 4 h after termination of infusion for cows that received 3 mg of NA/h per kilogram of BW. Experiment 2 was a 5 × 5 Latin square with 7-d periods and 9 recovery days between each period. Each period consisted of 5 d of partial feed restriction to increase plasma NEFA concentration. Treatments were continuous abomasal infusion of 0, 0.5, 1, or 3 mg of free NA/h per kilogram of BW for 4.5 d starting at feed restriction or 0.5 mg of NA/h per kilogram of BW infused directly into the rumen in a form protected from microbial degradation. The ruminal administration of protected NA was initiated 2 d before abomasal infusions and initiation of feed restriction to establish steady postruminal delivery of NA by start of abomasal infusions. Plasma NEFA was approximately 70 μEq/L before initiation of feed restriction and increased to 509, 587, 442, 850, and 108 μEq/L at 4.5 d for cows that received 0, 0.5 (protected NA), 0.5 (free NA), 1, and 3 mg of NA/h per kilogram of BW, respectively. An antilipolytic response was achieved with the highest abomasal dose, which maintained plasma NEFA concentration lower than the control group. An increase in plasma NEFA concentration was observed after termination of infusions for cows that received 1 and 3 mg of NA/h per kilogram of BW. Plasma NEFA was 1,900 μEq/L at 4 h after termination of infusion for cows receiving 1 mg of NA/h per kilogram of BW and 1,360 μEq/L at 5 h after termination of infusion for cows receiving 3 mg of NA/h per kilogram of BW. In nongestating, nonlactating cows it is unlikely that a dose of NA exists that will reduce plasma NEFA concentration and prevent the rebound that occurs following termination of NA administration.