Cardiovascular effects produced by injections of thyrotropin-releasing hormone in specific preoptic and hypothalamic nuclei in the rat.

Microinjection of 1.4 pmol TRH (0.5 ng; 50-150 nl) into both the preoptic suprachiasmatic nucleus (pos) and the A7000-6800 region of the medial preoptic nucleus (pom) produced increases in blood pressure and heart rate of 7% and 19%, respectively; heart rate responses in these two areas were higher than those occurring in other areas tested. TRH induced a significant increase in blood pressure and heart rate in the posterior hypothalamic nucleus (nhp) and increased heart rate only in the anterior (nha) and dorsomedial (ndm) hypothalamic nuclei. A small decrease in both blood pressure and heart rate resulted with TRH injections in the A7400-7050 region of the pom. No changes in respiratory rate or rectal temperature were observed at any site with this dose of TRH. Preliminary studies into the mechanism of the cardiovascular actions of TRH suggested that inhibition of the parasympathetic nerves to the heart make a partial contribution to the TRH-induced heart rate increase in the pos and that adrenal catecholamine release mediates the TRH response in the nhp. Neither methylatropine pretreatment nor adrenalectomy prevented the response to TRH injected into the nha, suggesting that activation of the cardiac sympathetic nerves may mediate TRH actions in this region. In the ndm, neither methylatropine nor adrenalectomy prevented the response to TRH; however, there was a tendency for the response to be less after methylatropine. Therefore, both inhibition of the parasympathetic and activation of the sympathetic nervous systems may contribute to the response observed, but no adrenal involvement could be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)