Neuroendocrine, sympathetic and metabolic responses induced by interleukin-1 Export

@article{berkenbosch89neuroendocrine, abstract = {1: Neuroendocrinology. 1989 Nov;50(5):570-6. LinksNeuroendocrine, sympathetic and metabolic responses induced by interleukin-1.Berkenbosch F, de Goeij DE, Rey AD, Besedovsky HO.Department of Pharmacology, Medical Faculty, Free University, Amsterdam, The Netherlands.Effects on turnover of vasopressin (AVP) in the hypothalamus and on secretion of pituitary hormones, catecholamines and insulin after intraperitoneal injection of recombinant interleukin-1 (beta) (IL-1) were investigated in male wistar rats. Intraperitoneal administration of IL-1 in a dose (1 microgram) that maximally activated pituitary-adrenal activity failed to alter plasma concentrations of prolactin, luteinizing hormone and melanocyte-stimulating hormone. Rats chronically cannulated in the right jugular veins showed a time-related increase in plasma corticosterone concentrations in response to intraperitoneal administration of IL-1 that lasted up to 4 h. In the same rats, plasma epinephrine (E) and norepinephrine (NE) concentrations were only slightly elevated (2-fold increase) at 30 min and at 1 h after IL-1 administration. Unlike in endotoxin-resistant C3H/HeJ mice, where IL-1 induces hypoglycemia, IL-1 did not affect plasma concentrations of glucose and insulin in Wistar rats. In the zona externa of the median eminence, IL-1 stimulated corticotropin-releasing factor (CRF) turnover at an approximate rate of 15\%/h, but did not cause a concomitant change in AVP turnover as can be observed after insulin-induced hypoglycemia. Since half of the hypothalamic CRF neurons have been shown to costore AVP, the data favor the view of a selective effect of IL-1 on a subtype of CRF neurons. We conclude that pituitary-adrenal activation in response to Il-1 is caused by CRF secretion from a subtype of CRF neurons (not storing AVP) in the rat hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)}, author = {Berkenbosch, F. and de Goeij, D. E. C. and Del Rey, A. and Besedovsky, H. O.}, citeulike-article-id = {4284288}, journal = {Neuroendocrinology}, keywords = {file-import-09-04-07}, number = {5}, pages = {570--6}, posted-at = {2009-04-07 13:55:23}, priority = {2}, publisher = {Karger}, title = {{Neuroendocrine, sympathetic and metabolic responses induced by interleukin-1}}, volume = {50}, year = {1989} }

TY - JOUR ID - berkenbosch89neuroendocrine L3 - citeulike-article-id:4284288 N2 - 1: Neuroendocrinology. 1989 Nov;50(5):570-6. LinksNeuroendocrine, sympathetic and metabolic responses induced by interleukin-1.Berkenbosch F, de Goeij DE, Rey AD, Besedovsky HO.Department of Pharmacology, Medical Faculty, Free University, Amsterdam, The Netherlands.Effects on turnover of vasopressin (AVP) in the hypothalamus and on secretion of pituitary hormones, catecholamines and insulin after intraperitoneal injection of recombinant interleukin-1 (beta) (IL-1) were investigated in male wistar rats. Intraperitoneal administration of IL-1 in a dose (1 microgram) that maximally activated pituitary-adrenal activity failed to alter plasma concentrations of prolactin, luteinizing hormone and melanocyte-stimulating hormone. Rats chronically cannulated in the right jugular veins showed a time-related increase in plasma corticosterone concentrations in response to intraperitoneal administration of IL-1 that lasted up to 4 h. In the same rats, plasma epinephrine (E) and norepinephrine (NE) concentrations were only slightly elevated (2-fold increase) at 30 min and at 1 h after IL-1 administration. Unlike in endotoxin-resistant C3H/HeJ mice, where IL-1 induces hypoglycemia, IL-1 did not affect plasma concentrations of glucose and insulin in Wistar rats. In the zona externa of the median eminence, IL-1 stimulated corticotropin-releasing factor (CRF) turnover at an approximate rate of 15%/h, but did not cause a concomitant change in AVP turnover as can be observed after insulin-induced hypoglycemia. Since half of the hypothalamic CRF neurons have been shown to costore AVP, the data favor the view of a selective effect of IL-1 on a subtype of CRF neurons. We conclude that pituitary-adrenal activation in response to Il-1 is caused by CRF secretion from a subtype of CRF neurons (not storing AVP) in the rat hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS) IS - 5 JF - Neuroendocrinology EP - 6 TI - {Neuroendocrine, sympathetic and metabolic responses induced by interleukin-1} PB - Karger VL - 50 SP - 570 KW - file-import-09-04-07 AU - Berkenbosch, F AU - de Goeij, DEC AU - Del Rey, A AU - Besedovsky, HO PY - 1989/// ER -