Effect of anterior pituitary perfusion and intraventricular injection of catecholamines and indoleamines on LH release

The median eminence, pituitary stalk and anterior pituitary as well as the adjacent diencephalon were exposed through a parapharyngeal approach to enable us to visualize these structures directly and to inject isotonic salt solutions containing dopamine, epinephrine, norepinephrine, serotonin or melatonin into the third ventricle, a stalk portal vessel or the basilar artery of anesthetized male rats. The rate of LH release in these animals was evaluated from the changes in the concentration of serum LH as determined by radioimmunoassay. Within 10 min after 1.25 μg of dopamine hydrochloride was injected into the third ventricle, the serum LH concentration had increased 4-fold. After 20 min, the serum LH level had increased 9-fold. At 30 and 60 min after the injection, there was a moderate decline followed by a steady rise for at least 1 hr. At the end of the 120-min observation period, the serum LH level was 20 times greater than that of the control animals which received an isotonic salt solution only. For quantities of dopamine greater than 1.25 μg, the resulting serum LH levels were inversely related to the dosage, e.g., 20 min after the injection of 1.25, 2.5, 5, 10 and 100 μg of dopamine hydrochloride, the mean serum LH concentrations were 19.4, 16.9, 13.4, 10.3 and 1.3 ng/ml, respectively. A similar response pattern Intraventricular injection of 2.5 and 5 ng of epinephrine or norepinephrine bitartrate did not affect LH release although the injection of 100 μg did do so. The intraventricular injection of serotonin creatinine sulfate complex hydrate in doses of 2.5 and 5 μg or the injection of melatonin in doses of 1, 5 and 50 μg caused statistically significant decreases in the concentration of LH in serum during the first hour after the administration of each indoleamine. When dopamine, epinephrine, norepinephrine, serotonin or melatonin was perfused into the anterior pituitary for 30 min via a microcannula inserted into a hypophysial portal vein, LH release was not affected. Furthermore, when dopamine was infused into the stalk-median eminence complex via the basilar artery, no significant effect on the serum LH concentration was observed. The values for serum LH in rats infused with dopamine via the basilar artery did not differ significantly from those obtained in animals infused with dopamine by way of a stalk portal vessel. These findings indicate that neither dopamine, epinephrine, norepinephrine, serotonin nor melatonin affected LH release by a direct action on the anterior pituitary but indirectly through the hypothalamic-hypophysial complex.