interleukin-1 and hypothalamic-pituitary-adrenal axis: negative feedback circuitry between immune...

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249 Adrenergic innervation of mesenteric arteries in wistar-kyoto rats, spontaneously hypertensive rats and rats treated with monosodium glutamate Yoshihisa Kawase, Saburo Shikuwa, Kazuko Shichijo, Masahiro Ito and Ichiro Sekine Department of Pathology, Atomic Disease Institute, Nagasaki Unioersity, School of Medicine, Nagasaki, Japan The adrenergic innervation of mesenteric arteries of Wistar-Kyoto rats, spontaneously hypertensive rats, and rats treated at birth with monosodium glutamate, was investigated by glyoxylic acid fluorescence histochemistry, by quantitative analysis, and by assaying catecholamine content by high performance liquid chromatography. Fluorescence histochemistry revealed that the plexus density of fluorescent fibres and the norepinephrine content were significantly higher in mesenteric arteries of hypertensive rats than in Wistar-Kyoto rats. In contrast, the plexus density was reduced in mesenteric arteries of rats treated with glutamate, although the catecholamine content was not changed. This study suggests that there is an increase in adrenergic activity in the mesenteric arteries of hypertensive rats, whereas in those of rats treated with glutamate there may be a reduction of sympathetic activity. (The Autonomic Nervous System, 26: 463-468, 1989) Interleukin-I and hypothalamic-pituitary-adrenal axis: negative feedback circuitry between immune and endocrine systems Akira Uehara, Toshikatsu Okumura, Chihiro Sekiya, Yuichi Takasugi and Masayoshi Namiki Department of Internal Medicine (III), Asahikawa Medical College, Asahikawa, Japan It is becoming increasingly evident that there is reciprocal communication between the immune and the endocrine systems. Hormones and neuropeptides affect immune functions, and, in turn, immune responses are reflected in neuroendocrine changes. The present study was conducted to determine, i. the effect of interleukin-1 (IL-1), a polypeptide produced by stimulated monocytes/macrophages, on the hypo- thalamic-pituitary-adrenal axis, and, ii. the effect of glucocorticoid hormones on the release of IL-1 from human peripheral blood mononuclear cells in culture. Intravenous injection of IL-1 into freely moving, conscious rats increased several folds the plasma level of ACTH. The response was dose related and peaked 10 min after injection. The response was completely inhibited by previous injection of 0.5 ml of rabbit antiserum generated against rat corticotropin-releasing factor, but not by normal rabbit serum. IL-1 failed to stimulate the release of ACTH from primary monolayer cultures of rat anterior pituitary cells in concentrations ranging from 0.001 to 100 nm. Prednisolone, a water-soluble synthetic glucocorticoid hormone, suppressed in a dose-related manner the secretion of IL-1 from cultured blood cells. This effect occurred at low concentration of prednisolone: 50% inhibition was observed at 0.1 nm. (The Autonomic Nervous System, 26: 469-475, 1989)

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Page 1: Interleukin-1 and hypothalamic-pituitary-adrenal axis: negative feedback circuitry between immune and endocrine systems

249

Adrenergic innervation of mesenteric arteries in wistar-kyoto rats, spontaneously hypertensive rats and rats treated with monosodium glutamate

Yoshihisa Kawase, Saburo Shikuwa, Kazuko Shichijo, Masahiro Ito and Ichiro Sekine

Department of Pathology, Atomic Disease Institute, Nagasaki Unioersity, School of Medicine, Nagasaki, Japan

The adrenergic innervation of mesenteric arteries of Wistar-Kyoto rats, spontaneously hypertensive rats, and rats treated at birth with monosodium glutamate, was investigated by glyoxylic acid fluorescence histochemistry, by quantitative analysis, and by assaying catecholamine content by high performance liquid chromatography. Fluorescence histochemistry revealed that the plexus density of fluorescent fibres and the norepinephrine content were significantly higher in mesenteric arteries of hypertensive rats than in Wistar-Kyoto rats. In contrast, the plexus density was reduced in mesenteric arteries of rats treated with glutamate, although the catecholamine content was not changed. This study suggests that there is an increase in adrenergic activity in the mesenteric arteries of hypertensive rats, whereas in those of rats treated with glutamate there may be a reduction of sympathetic activity.

(The Autonomic Nervous System, 26: 463-468, 1989)

Interleukin-I and hypothalamic-pituitary-adrenal axis: negative feedback circuitry between immune and endocrine systems

Akira Uehara, Toshikatsu Okumura, Chihiro Sekiya, Yuichi Takasugi and Masayoshi Namiki

Department of Internal Medicine (III), Asahikawa Medical College, Asahikawa, Japan

It is becoming increasingly evident that there is reciprocal communication between the immune and the endocrine systems. Hormones and neuropeptides affect immune functions, and, in turn, immune responses are reflected in neuroendocrine changes. The present study was conducted to determine, i. the effect of interleukin-1 (IL-1), a polypeptide produced by stimulated monocytes/macrophages, on the hypo- thalamic-pituitary-adrenal axis, and, ii. the effect of glucocorticoid hormones on the release of IL-1 from human peripheral blood mononuclear cells in culture. Intravenous injection of IL-1 into freely moving, conscious rats increased several folds the plasma level of ACTH. The response was dose related and peaked 10 min after injection. The response was completely inhibited by previous injection of 0.5 ml of rabbit antiserum generated against rat corticotropin-releasing factor, but not by normal rabbit serum. IL-1 failed to stimulate the release of ACTH from primary monolayer cultures of rat anterior pituitary cells in concentrations ranging from 0.001 to 100 nm. Prednisolone, a water-soluble synthetic glucocorticoid hormone, suppressed in a dose-related manner the secretion of IL-1 from cultured blood cells. This effect occurred at low concentration of prednisolone: 50% inhibition was observed at 0.1 nm.

(The Autonomic Nervous System, 26: 469-475, 1989)