It is well established that heat stress during mid- and late-gestation induces intrauterine growth retardation (IUGR) and decreased milk yield in the subsequent lactation in cattle and sheep. We hypothesized that elevated fetal adrenal norepinephrine (NE) secretion contributes to impaired mammary development in heat stressed pregnant ewes. Pregnant ewes were assigned to one of 4 treatment groups that were a combination of control (C) or hyperthermia-induced IUGR (I) and surgical sham (S) or bilateral fetal adrenal demedullation (D) at 98 d gestational age (dGA; term = 148 dGA)(n = 4 CS, 4 CD, 6 IS, and 4 ID fetuses). At 134 dGA, fetal plasma NE was measured, animals were euthanized, and fetal and placental weights obtained. Ewes’ mammary glands were collected, weighed and prepared for analyses of DNA content, and histological evaluation to quantify the numbers of alveolar units per microscopic field and mammary epithelial cells per alveolus. Data were analyzed by Proc Mixed ANOVA, SAS 9.3. In the IS group, fetal plasma NE was 4-fold higher (P < 0.05) and placental, fetal and maternal mammary weights and mammary DNA were lower (P < 0.05) compared with the CS group and these parameters were partially reversed in the ID group. Placental weight: CS 337 ± 34, CD 271 ± 39, IS 160 ± 36, ID 215 ± 50 g; Fetal weight: CS 3495 ± 214, CD 3343 ± 233, IS 1746 ± 330, ID 2574 ± 296 g; Mammary wet weight: CS 3043 ± 445, CD 2496 ± 345, IS 785 ± 300, ID 1326 ± 316 g; Mammary dry weight: CS 343 ± 34, CD 353 ± 59, IS 192 ± 44, ID 278 ± 58 g; Mammary DNA content: CS 3043 ± 456, CD 2946 ± 353, IS 868 ± 353, ID 1327 ± 322 ng/µl. There were no treatment effects on the number of alveolar units per field: CS 33.6 ± 9.6, CD 17.3 ± 4.0, IS 16.5 ± 5.0, ID 28.5 ± 3.9; or number of cells per alveolus: CS 6.5 ± 1.0, CD 7.5 ± 2.0, IS 8.2 ± 0.3, ID 6.4 ± 1.0. We conclude that heat stress during gestation reduces placental, fetal and mammary development and fetal adrenal de-medullation partially reverses these effects. We also propose that an endocrine signal from the placenta regulates maternal mammary growth during gestation and this signal is responsive to fetal catecholamines.