Masanori Sugawara
Okayama University
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Featured researches published by Masanori Sugawara.
Regulatory Peptides | 1988
Kozo Hashimoto; Shuso Suemaru; Toshihiro Takao; Masanori Sugawara; Shinya Makino; Ota Zensuke
Brain corticotropin-releasing hormone (CRH) concentration and pituitary adreno-cortical responses were examined in chronically stressed rats: body restraint stress (6 h/day) for 4 or 5 weeks. Stressed rats showed a reduction in weight gain. CRH concentration in the median eminence and the rest of the hypothalamus were not different between control and chronically immobilized rats. The anterior pituitary adenocorticotropic hormone (ACTH) concentration was elevated in chronically stressed rats, whereas plasma ACTH and corticosterone levels did not differ from the control values. The median eminence CRH concentration was reduced to the same extent at 5 min after onset of ether exposure (1 min) in chronically immobilized rats and controls. However, plasma ACTH and corticosterone showed greater responses to ether stress in chronically immobilized rats than in control rats. Plasma ACTH and corticosterone responses to exogenous CRH were not different between control and chronically immobilized rats, while the response to arginine vasopressin (AVP) was significantly greater in chronically immobilized rats. These results suggest that chronic stress caused an increase in the ACTH-secreting mechanism and that pituitary hypersensitivity to vasopressin might at least be partly responsible for this.
Regulatory Peptides | 1987
Kozo Hashimoto; Teruhiko Hattori; Shuso Suemaru; Masanori Sugawara; Toshihiro Takao; Jingo Kageyama; Zensuke Ota
The effect of synthetic atrial natriuretic peptide (ANP) was examined on the in vivo and in vitro release of ACTH. Intravenous ANP (4 micrograms/kg body weight) administration did not affect the corticotropin releasing factor (CRF, 4 micrograms/kg body weight)-, arginine vasopressin (AVP, 2 micrograms/kg body weight)- and angiotensin II (A II, 4 micrograms/kg body weight)-induced ACTH release in unanesthetized freely moving rats. ANP did not inhibit the basal, CRF- and AVP-induced release of ACTH in pituitary cell cultures. ANP did not affect the CRF- and AVP-induced plasma corticosterone elevation, while it attenuated the AVP-induced corticosterone elevation. These results indicate that ANP does not affect the ACTH release at the pituitary level in vivo and in vitro.
Peptides | 1987
Kozo Hashimoto; Shuso Suemaru; Norihito Ono; Teruhiko Hattori; Hiroshi Inoue; Toshihiro Takao; Masanori Sugawara; Jingo Kageyama; Zensuke Ota
An intra-third ventricular administration of (D-Ala2,Met5)-enkephalinamide (DALA) did not elevate plasma ACTH and corticosterone levels in unanesthetized freely moving rats, but intra-third ventricular administration of DALA and methionine (Met)-enkephalin potentiated a mild stress (hanging for 10 or 30 sec)-induced plasma ACTH and corticosterone elevations in unanesthetized freely moving rats. DALA and Met-enkephalin seemed to stimulate CRF release from the median eminence to increase plasma ACTH, as the CRF concentration in the median eminence area was reduced after injection in these stressed rats. When hypothalamic tissues were perifused in vitro, DALA (1-100 ng/ml) reduced the release of CRF. These results suggest that the opiates seem to have a dual effect on the CRF-ACTH system depending on which action overrides the other.
Journal of Clinical Investigation | 1988
Kozo Hashimoto; Shuso Suemaru; Toshihiro Takao; Masanori Sugawara; Teruhiko Hattori; Jingo Kageyama; Kayo Takahashi; Zensuke Ota
1.0 micrograms/kg body wt human corticotropin-releasing factor (hCRF) and 0.005 IU/kg body wt lysine vasopressin (LVP) were administered in a bolus dose to patients receiving daily or alternate-day glucocorticoid therapy. In normal subjects with this hCRF-LVP test, the plasma ACTH increment was significantly greater (approximately 2.5-fold) 15 min after injection than under the CRF test. In patients receiving daily glucocorticoid therapy (greater than 15 mg prednisolone or an equivalent daily dose), the plasma ACTH and cortisol responses to hCRF-LVP were suppressed 2 wk to 1 mo after the beginning of glucocorticoid administration but partially improved at 2-10 mo, and was markedly suppressed several years later. On the other hand, in patients receiving alternate-day glucocorticoid therapy, the plasma ACTH response was normal at 2 wk, normal or higher at 1-3 mo, and normal after 4 mo. A normal plasma cortisol response was observed throughout the test period in patients receiving alternate-day therapy after pulse therapy, whereas plasma cortisol response was gradually improved in patients receiving alternate-day therapy after several months of daily therapy.
Journal of Neuroendocrinology | 1989
Toshihiro Takao; Kozo Hashimoto; Ryuto Hirasawa; Shinya Makino; Masanori Sugawara; Kazuharu Murakami; Zensuke Ota
Plasma ACTH increased after an intra‐third ventricular administration of noradrenaline (NA). An iv corticotrophin‐releasing factor (CRF) antagonist [alpha‐helical CRF(9–41)] injection did not affect ACTH secretion by itself, whereas it significantly reduced NA‐induced ACTH secretion. These results suggest that NA centrally stimulated ACTH secretion and that endogenous CRF is involved in this ACTH secretion.
Endocrinology | 1989
Kozo Hashimoto; Shinya Makino; Ryuto Hirasawa; Toshihiro Takao; Masanori Sugawara; Kazuharu Murakami; Katsuhiko Ono; Zensuke Ota
Acta Medica Okayama | 1989
Kozo Hashimoto; Kazuharu Murakami; Toshihiro Takao; Shinya Makino; Masanori Sugawara; Zensuke Ota
Endocrinologia Japonica | 1988
Masanori Sugawara; Kozo Hashimoto; Teruhiko Hattori; Toshihiro Takao; Shuso Suemaru; Zensuke Ota
European Journal of Endocrinology | 1986
Kozo Hashimoto; Shuso Suemaru; Teruhiko Hattori; Masanori Sugawara; Zensuke Ota; Shinji Takata; Kazuo Hamaya; Kenji Doi; Michel Chrétien
Endocrinologia Japonica | 1986
Teruhiko Hattori; Kozo Hashimoto; Hiroshi Inoue; Masanori Sugawara; Shuso Suemaru; Jingo Kageyama; Zensuke Ota