{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T18:58:16Z","timestamp":1777921096509,"version":"3.51.4"},"reference-count":0,"publisher":"S. Karger AG","license":[{"start":{"date-parts":[[2008,4,9]],"date-time":"2008-04-09T00:00:00Z","timestamp":1207699200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"},{"start":{"date-parts":[[2008,4,9]],"date-time":"2008-04-09T00:00:00Z","timestamp":1207699200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuroendocrinology"],"abstract":"The purpose of these studies was to assess the involvement of \u03b2-adrenoceptors in the development of psychological stress-induced elevation in body temperature (Tb) and rise in circulating interleukin-6 (IL-6). We selected three drugs to attempt to block the rise in body temperature and plasma IL-6; L-propranolol, D-propranolol and nadolol. Both stereoisomers of propranolol have \u2018local anesthetic\u2019 membrane-stabilizing activity and are capable of penetrating into the brain. However, D-propranolol has significantly lower \u03b2-blocking activity than L-propranolol. Nadolol has \u03b2-blocking activity similar to L-propranolol without membrane-stabilizing activity. Furthermore, nadolol does not cross the blood-brain barrier. All \u03b2-blockers were injected intraperitoneally (i.p. 7.5 mg\/kg) or into the third cerebral ventricle (i.c.v., 5 or 50 \u00b5g\/animal), 20 min or just before exposure of rats to an open field, respectively. Blood samples for measurement of plasma IL-6 activity (IL-6-dependent B9 cell bioassay) were taken from rats immediately following exposure to the open field. After exposure to the open field, rats not treated with \u03b2-blockers responded with a rapid rise in T<sub>b<\/sub> measured by biotelemetry as well as with an increase in plasma IL-6 activity. The increase in T<sub>b<\/sub> of open field-exposed rats was significantly suppressed by L-propranolol injected i.p. (\u0394T<sub>max<\/sub> = 0.14 \u00b1 0.15\u00b0C for L-propranolol vs. 0.78 \u00b1 0.15\u00b0C for vehicle-treated rats). Neither i.p. injection of D-propranolol nor nadolol had any effect on the increase in T<sub>b<\/sub> induced by exposure to the open field. Both i.c.v. doses of L-propranolol and nadolol markedly attenuated the open field-induced rise in T<sub>b<\/sub>. The large i.c.v. dose of D-propranolol (50 \u00b5g) did, whereas the lower dose (5 \u00b5g) did not suppress the elevation in T<sub>b<\/sub> in open field exposed rats. The open field-exposed rats injected with L-propranolol (both i.p. or i.c.v.) had lower plasma IL-6 activity than that of open field-exposed rats injected with vehicle (for i.p. injection: 5.2 \u00b1 1.3 U\/ml for L-propranolol vs. 17.4 \u00b1 3.8 U\/ml for vehicle; for i.c.v. injection: 3.5 \u00b1 2.3 U\/ml for L-propranolol vs. 24.4 \u00b1 7.2 U\/ml for vehicle). Nadolol blocked the open field-induced rise in plasma IL-6 only when injected i.c.v. but not i.p. Neither i.p. nor i.c.v. D-propranolol injection had an effect on plasma IL-6 activity in open field-exposed rats. These data show that \u03b2-adrenoceptors in the central nervous system are involved in the psychological stress-induced elevation in T<sub>b<\/sub> and rise in plasma IL-6 activity caused by exposure to an open field.<\/jats:p>","DOI":"10.1159\/000127072","type":"journal-article","created":{"date-parts":[[2008,4,10]],"date-time":"2008-04-10T04:37:20Z","timestamp":1207802240000},"page":"459-467","source":"Crossref","is-referenced-by-count":60,"title":["Beta-Adrenoceptor Antagonists Suppress Elevation in Body Temperature and Increase in Plasma IL-6 in Rats Exposed to Open Field"],"prefix":"10.1159","author":[{"given":"Dariusz","family":"Soszynski","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wieslaw","family":"Kozak","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carole A.","family":"Conn","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karin","family":"Rudolph","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew J.","family":"Kluger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2008,4,9]]},"container-title":["Neuroendocrinology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/127072","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/karger.com\/article-pdf\/doi\/10.1159\/000127072","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T19:45:21Z","timestamp":1777664721000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000127072"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2008,4,9]]},"references-count":0,"URL":"https:\/\/doi.org\/10.1159\/000127072","archive":["Portico"],"relation":{},"ISSN":["0028-3835","1423-0194"],"issn-type":[{"value":"0028-3835","type":"print"},{"value":"1423-0194","type":"electronic"}],"subject":[],"published":{"date-parts":[[2008,4,9]]}}}