Abstract
The physiological importance of somatostatin in the control of growth hormone (GH) secretion is indicated by the observation of a 10-fold stimulation of plasma GH levels 5 minutes after intravenous injection of somatostatin antiserum. It thus appears that under basal conditions, GH secretion is 90–95% inhibited by somatostatin. Maintenance of the episodic bursts of GH release in the presence of excess somatostatin antiserum indicates intermittent release of GH-releasing activity (GH-RH) from the hypothalamus. The stimulatory effect of morphine observed in the presence of excess circulating somatostatin antibodies indicates that the narcotic exerts its action through increased GH-RH release and not inhibition of somatostatin secretion. When injected intracerebrally, methionine-enkephalin (β-LPH61–65) and β-endorphin (β-LPH61–91) stimulate both GH and prolactin (PRL) release, the effect on PRL release being observed at shorter time intervals after injection and at lower doses of the peptides. β-endorphin is, however, 500 to 2000 times more potent than met-enkephalin. The analogs (D-Ala2) met-enkephalin-NH2 and met-enkephalinethylamide are 500 to 1500 times more potent than met-enkephalin itself on both GH and PRL release. At the 1 mg dose, (D-Ala2) met-enkephalin can stimulate the release of the two pituitary hormones by parenteral injection.