Growth Hormone Releasing Activity of Thyrotropin-Releasing Hornione in Rats with Hypothalamic Lesions12

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Abstract
The growth hormone (GH)-releasing effect of thyrotropin-releasing hormone (TRH) was investigated in rats in which CNS-anterior pituitary (AP) connections were experimentally interrupted. Sprague-Dawley (SD) female and male rats underwent bilateral electrolytic lesions in the median eminence (ME) or the ventromedial nuclei (VMN) or were sham-operated (sham-op). Fifteen days after surgery, 0.9% NaCl or TRH was injected i.v. into sham-op rats or those with lesions in the CNS, anesthetized with urethane, and blood was drawn at 5 and 10 min posttreatment. In the rats with ME lesions, TRH at all the doses used (0.1, 0.4 and 0.8 .mu.g/100 g BW [body weight]) induced a marked, although not dose-related GH rise, which was not present in sham-op rats after TRH, or after NaCl administration to either rats with ME lesions or sham-op rats. In SD male rats lesioned in the VMN, TRH at doses of 0.4 and 0.8 .mu.g/100 g BW induced significant GH rises, while the lowest TRH dose (0.1 .mu.g/100 g BW) was ineffective; again, TRH was ineffective at all doses used in sham-op rats. Concomitant evaluation of the prolactin (PRL)-releasing effect of TRH (0.1-0.8 .mu.g/100 g BW), showed a striking elevation of plasma PRL in both female and male sham-op controls, but no PRL rise in the rats with ME lesions. In the rat with surgical separation of the anterior pituitary from the CNS, a direct GH-releasing effect of TRH can be obtained, whereas its PRL-releasing effect is no longer observed, and suggest that, by analogy, the GH-releasing effect of TRH present in some disease states of the human may be due to an impairment of CNS-AP connections.