Somatostatin is a regulator of thyrotropin secretion in the perinatal rat.

The perinatal rat exhibits low serum TSH levels in the presence of very low concentrations of T3 and T4. We had reported previously that this animal does not require endogenous TRH for TSH release. We investigated here whether the inhibitory hormone somatostatin (SS) has a role in maintaining the low TSH secretory set-point. To study the effect of SS in the immature model, we passively immunized pregnant rats with SS antiserum to neutralize endogenous SS. Acute iv administration of 0.3 ml SS antiserum to pregnant rats (day 20 of pregnancy) resulted in a significant serum TSH elevation in both mother and fetus 60 min after injection compared to the control values [maternal TSH, 62 +/- 6 muU/ml vs. control, 43 +/- 4 (mean +/- SE; P less than 0.05); fetal TSH, 95 +/- 8 vs. control, 66 +/- 6 (P less than 0.02)]. The binding capacity of the AS in the fetal serum far exceeded the circulating SS in the fetus. Similar results were obtained when neonates 5 and 10 days of age were injected with 0.1 ml AS, ip. Further experiments were done with the use of synthetic SS. Acute iv injection of synthetic synthetic SS (1 microgram) to pregnant rats made hypothyroid by feeding of a low iodine-propylthiouracil diet for the last week of gestation suppressed the elevated serum TSH level in both mother and fetus 15 min after the injection [maternal TSH, 102 +/- 11 vs. control, 163 +/- 22 (P less than 0.05); fetal TSH, 99 +/- 9 vs. control, 143 +/- 13 (P less than 0.02)]. Similar results were obtained when hypothyroid neonates 5 and 10 days of age were injected with 1 microgram SS, ip. These findings suggest that there is similarity in the effects of SS on TSH secretion (suppression) in mother, fetus, and neonate and dependence of the perinatal TSH on SS, in contrast to TRH. It is, then, likely that TSH secretion in the perinatal rat is under the inhibitory influence of endogenous SS.