Abstract
To investigate the secretory mechanism of growth hormone (GH) in rat, plasma GH levels under diverse experimental conditions were determined by radioimmunoassay.
All studies were carried out with male Wistar rats (200-250 g). The rats were housed, 6 per cage, in the room under constant temperature and light-dark cycles.
Plasma GH levels in gentled rats were significantly higher than those in nongentled rats. Basal plasma GH levels were considerably fluctuated over a wide range of values. No statistically significant diurnal variation in plasma GH were demonstrated, although the lowest GH levels were generally observed at 5 p.m. and corresponded to peak values for plasma corticosterone. Pentobarbital (PB) anesthesia caused a significant rise in plasma GH in both gentled and non-gentled rats. On the other hand, many stimuli provided with much stress, such as ether anesthesia, insulin induced hypoglycemia, hypertonic glucose, 2-deoxyglucose and catheterization, resulted in a marked suppression of plasma GH. Chronic administration of reserpine accentuated the effect of insulin. All of these suppressive effects of various stresses on plasma GH were blocked partially or totally by PB anesthesia except the case of catheterization. Intensity of the stress produced by catheterization seemed to be higher than that by other stimuli provided with much stress.
Dexamethasone also caused a marked decrease in plasma GH even under PB anesthesia. This fact indicated that GH and ACTH release were regulated independently, although in many cases, GH suppression was accompanied by an increase in plasma corticosterone. Furthermore, it suggested that suppression of GH release could be caused by some other factors than stress.
Neither arginine nor vasopressin infused into the carotid artery in PB anesthetized rat affected plasma GH concentration at all. Although in the first experiment, dibutyryl cyclic AMP infused through the same route together with aminophylline caused an increase in plasma GH level, no effect of the same combination was demonstrated in the second experiment. The results obtained from infusion of SME extract were also not reproducible. In the first experiment with crude extract, a significant rise of plasma GH concentration was observed. However, in both of the 2 nd and the 3 rd experiments, no increment in plasma GH level was observed. It is too early at the present time to decide whether these test materials were inactive or the method was insensitive.
The results of the present study confirmed that the secretion pattern of GH in rat is quite unique and that a variety of stimuli provided with much stress depress plasma GH in the rat in contrast to their stimulatory effect in other species.
