Plasma GH levels of fed male gentled rats (52+6 ng/ml) were significantlygreater than those of nongentled animals (24 + 5 ng/ml). Plasma corticosterone levels showed the opposite relationship—gentled, 4.6 ± 0.8 μg/100 ml, vs. nongentled, 8.4 ± 1.4 μg/100 ml. Pentobarbital anesthesia caused a significant rise in plasma GH in both gentled and nongentled rats and a corresponding decrease in plasma corticosterone. A statistically significant diurnal variation in plasma GH could not be demonstrated, although the lowest GH levels were generally observed at 5 PM and corresponded to peak values for plasma corticosterone. Ether anesthesia, hypertonic glucose, 2-deoxyglucose, insulin-induced hypoglycemia and epinephrine all resulted in a marked suppression of plasma GH, and an increase in plasma corticosterone, effects which were either partially or completely blocked by pentobarbital anesthesia. The effects of insulin-induced hypoglycemia and 2-deoxyglucose were not mediated by catecholamines since they were noted in adrenalectomized animals and the response was not abolished by depletion of endogenous catecholamines with reserpine. Femoral venous catheterization consistently and rapidly suppressed the plasma GH and this inhibitory effect was not blocked by pentobarbital anesthesia. (Endocrinology88: 909, 1971)
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Takahashi et al. (1971) studied this question.