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Physiologically Significant Effect of Neuropeptide Y to Suppress Growth Hormone Release by Stimulating Somatostatin Discharge^*

Department of Physiology, Neuropeptide Division, The University of Texas Southwestern Medical Center at Dallas Dallas, Texas 75235–9040

Address all correspondence and requests for reprints to: S. M. McCann, Department of Physiology, Neuropeptide Division, The University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75235-9040.

Abstract

Neuropeptide Y (NPY) is a peptide found in a variety of hypothalamic loci which is frequently colocalized with catecholamines. It is also secreted into hypophyseal portal vessels. The injection of NPY into the third ventricle (3V) lowered plasma GH levels in conscious, freely moving male rats. To determine the physiological significance of the hypothalamic inhibitory action of the peptide, highly specific antiserum directed against NPY was injected into the 3V of conscious rats. 3V injection of the antiserum evoked a significant elevation of plasma GH within 2 h on comparison to values in normal rabbit serum-injected, ovariectomized rats. The difference increased and reached a maximum at 6 h after injection. On the other hand, there was no effect of the antiserum in ovariectomized, estrogen, progesterone-blocked rats. Intraventricular injection of the anti-NPY serum also caused a significant elevation of plasma GH within 2 h in normal male rats and the increases above values in normal rat serum-injected control animals became even more significant at 3 and 4 h. To determine the mechanism by which NPY lowers GH after its intraventricular injection, its effect on the release of somatostatin (SRIF) from median eminence fragments incubated in vitro was examined. NPY stimulated SRIF release with a highly significant effect at a concentration of 10^-9 M. Borderline stimulation was observed at doses as low as 10¹¹ M. The curve was bell-shaped with a declining release at 10^-8 M and 10^-7 M. The releasing action of NPY was blocked by either the β-receptor blocker, prazosin (10^-6 M), or the ²-receptor blocker, propranolol (10^-6 M), but was not affected by the ²-receptor blocker, yohimbine (10^-6 M). We conclude that NPY has a physiologically significant inhibitory action within the hypothalamus to suppress GH release in ovariectomized female and intact male rats by stimulation of SRIF release by ¹ and β-adrenergic receptormediated mechanisms. (Endocrinology 126: 2296–2301,1990)

Footnotes

^* This work was supported by NIH Grants HD-09988 and DK-10073.

Received November 3, 1989.

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