Plasma thyrotrophin (TSH) response to intrahypothalamic injection of an α2-adrenergic receptor agonist (clonidine)

To delineate the site at which the central noradrenergic (NE) system may exert its stimulatory influence on the thyrotrophin (TSH) secretion, plasma TSH concentrations were measured before and after clonidine (an alpha 2-agonist) administration to the hypothalamus of unanaesthetized, unrestrained rats. When the animals received a simultaneous injection of clonidine (0.2 microgram) and phenoxybenzamine (2.0 micrograms) into the dorsomedial nucleus (DMN)/the paraventricular nucleus (PVN), a significant rise in TSH levels was observed. Injection of the mixture into the anterior hypothalamus, posterior hypothalamus, ventromedial hypothalamus, and arcuate nucleus had no influence on the plasma TSH concentration. Clonidine (10.0 micrograms/100 g body weight) and phenoxybenzamine (100 micrograms/100 g body weight) injected into the jugular vein also caused a prompt increase in the plasma TSH concentration. In rats with an intact small hypothalamic island, the TSH response to the iv injection of the drugs was considerably diminished. These data support the view that NE receptors in the DMN/PVN are of importance in exerting an NE-stimulatory influence on the TSH secretion, probably through the TRH neurons.