The impact of pregnancy on the counterregulatory response to insulin-induced hypoglycemia was examined in 6 nonpregnant (NP) and 6 pregnant (P; 3^rd trimester) conscious dogs using tracer and arteriovenous difference techniques. After basal sampling, insulin was infused intraportally at 30 pmol^.kg^-1.min^-1 for 180 min. Insulin rose from 7.0±15 to 158.6±221 pmol/l and 2.7±4 to 124.7±61 pmol/l in the 3rd h in NP and P, respectively. Arterial glucose fell from 5.9±0.2 to 2.3±0.2 mmol/l in P. Glucose was infused in NP to equate the rate of fall of glucose and the steady-state concentrations in the groups (5.9±0.2 to 2.3±0.1 mmol/l in NP). Glucagon was 32±6, 69±11, and 48±10 ng/l (basal, 1^st and 3^rd h) in NP, but the response was attenuated in P (34±5, 46±6, 41±9 ng/l). Cortisol and epinephrine rose similarly in both groups, but norepinephrine rose more in NP (3.01±0.46 and 1.31±0.13 nmol/l, P < 0.05). Net hepatic glucose output (NHGO; µmol^.kg^-1.min^{- 1}) increased from 10.6±1.8 to 21.2±3.3 in NP (3rd h), but did not increase in P (15.1±1.5 to 15.3±2.8 µmol^.kg^-1.min^-1, P < 0.05 between groups). The glycogenolytic contribution to NHGO in NP increased from 5.8±0.7 to 10.4±2.5 µmol^.kg^-1.min^-1 by 90 min, but steadily declined in P. The increase in glycerol levels and the gluconeogenic contribution to NHGO were 50% less in P than NP, but ketogenesis did not differ. The glucagon and norepinephrine responses to insulin-induced hypoglycemia are blunted in late pregnancy in the dog, impacting on the magnitude of the metabolic responses to the fall in glucose.