Pregnant ewes were chronically exposed to thermoneutral (TN; 20 degrees C, 30% relative humidity) or hot (H; 40 degrees C 9 h/d, 30 degrees C 15 h/d, 40% relative humidity) environments between d 64 and 136 to 141 of pregnancy. They were sampled for blood at 14-d intervals during this period for measurement of plasma metabolites and hormones, then slaughtered and dissected to measure conceptus weights, dimensions and fetal organ weights. Rectal temperatures of H ewes were elevated .3 to 1.0 C degrees above those of TN ewes throughout the experiment. Voluntary feed intakes were not altered by heat exposure except after 120 d of pregnancy, when feed intake was about 25% lower (P less than .10) by H than by TN ewes. Blood 3-hydroxybutyrate concentrations were not affected by heat, but plasma glucose concentrations were greater in H than in TN animals after 120 d (P less than .05). Placental weight, reduced by 54% (P less than .001) by heat exposure of ewes, was correlated positively with fetal weight and correlated negatively with fetal/placental weight ratio, fetal brain/liver weight ratio and fetal relative heart weight. Late in pregnancy, plasma concentrations of progesterone, cortisol and placental lactogen were reduced (P less than .01) in H ewes, whereas triiodothyronine levels were markedly lower (P less than .03) at all stages of pregnancy. Plasma concentrations of prolactin were elevated dramatically (P less than .01) and a modest increase (P less than .03) in somatotropin levels was recorded in H ewes. These results are consistent with our hypothesis that heat-induced fetal growth retardation is secondary to a primary reduction in placental growth; this could be mediated partly by reduced peripheral activity of thyroid hormones. Heat-induced reductions in secretion of progesterone and ovine placental lactogen more likely were a consequence than a cause of placental stunting.