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Biomedical subjects

M Hatano

Publications and source records attributed to M Hatano.

At least 235 records · Page 13Linked to original sources
PubMed1987

Abnormal response of adrenocorticotropin to corticotropin releasing factor in spontaneously hypertensive rats.

The pituitary-adrenocortical response to ovine corticotropin-releasing factor (CRF) was investigated in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) anesthetized with pentobarbital. After intravenous administration of various doses of CRF (0.1, 1.0 and 10 micrograms), the plasma levels of ACTH were significantly increased in both groups. ACTH increments after various doses of CRF were dose-dependent in WKY. ACTH increments after injections of 0.1, 1.0, and 10 micrograms of CRF in SHR were 123.2 +/- 36.5 (SE), 123.0 +/- 52.2 and 60.3 +/- 48.5 pg/ml at 5 min, and 386.3 +/- 73.8, 243.4 +/- 86.6 and 220.0 +/- 31.4 pg/ml at 15 min, respectively. The ACTH increments in SHR at 15 min after administration of 0.1 microgram of CRF were higher (p less than 0.02) than those in WKY. However, ACTH increments in SHR after administration of 10 micrograms of CRF were lower than those in WKY at 5 min (p less than 0.05) and 15 min. These data suggest that the plasma ACTH responses to various doses of CRF represent a dose-unrelated plateau response in SHR. The plasma levels of corticosterone after administration of various doses of CRF did not change significantly and there were no significant differences between the two strains. The results of these experiments suggest that SHR have an abnormal response of the pituitary-adrenocortical axis to CRF, and the abnormal response may be attributable to desensitization of the pituitary to CRF.

Adrenocorticotropic Hormone↗
PubMed1987

[Effect of platonin on bone wound healing in rat calvaria--with special reference to the interaction of platonin and steroid hormones].

Interaction of Platonin (PI) and dexamethasone (DM) or testosterone propionate (TP) on bone wound healing was studied by measuring the areas of wound holes which were made in the rat parietal bone. The result was compared with that of the growth of the femur. 1) No significant difference was observed between the control group and pl groups (1, 10 and 100 micrograms/kg, s.c., for 4 weeks) on the wound hole area or the length, weight, calcium content (Ca) or hydroxyproline content (HP) in the femur. 2) The bone wound healing was delayed by DM (2 mg/kg, s.c., for the first 2 weeks). The inhibition of growth was also observed in the femur length and weight, but no significant effect of DM was observed in the Ca and HP of the femur. The combination of Pl and DM promoted the recovery from delayed bone wound healing and femur weight gain caused by DM. 3) No significant effects of TP (4 mg/kg, s.c., for the first 2 weeks) were observed on the wound healing and the femur growth, but an increase of the femur weight and Ca was observed by the combination of Pl and TP. These results indicate that Pl promotes the recovery from delayed bone wound healing and femur weight gain by DM, although no significant effects were observed in bone growth and bone wound healing by the administration of Pl alone. It is also suggested that a combination of Pl and TP promotes bone growth and mineralization.

Animals↗
PubMed1987

Suppression of plasma aldosterone by chronic ACTH administration is offset by converting enzyme inhibitor.

In order to elucidate the mechanism of suppression of plasma aldosterone by chronic ACTH administration, especially the role of the renin-angiotensin system and dopamine, we administered ACTH with or without MK422, a converting enzyme inhibitor, to reduce the endogenous angiotensin II in rats, and measured the plasma renin activity, plasma corticoid concentrations and urinary dopamine excretion. The plasma aldosterone concentration (PAC) was decreased after chronic ACTH administration. However, in the ACTH + MK422 administered group, aldosterone suppression was not observed. It appeared therefore that the aldosterone suppressing mechanism was independent of the weakened renin-angiotensin system following chronic ACTH administration, since PAC was not decreased in the ACTH + MK422 administered group when angiotensin II might be completely eliminated. The urinary excretion of dopamine was significantly increased in the chronic ACTH + MK422 administered group as well as in the chronic ACTH administered group. This suggested that the inhibitory effect of dopamine on aldosterone did not contribute significantly to the suppression of plasma aldosterone. The present results suggest therefore that the mechanism of suppression of plasma aldosterone following chronic ACTH administration was not dependent on the renin-angiotensin system and dopamine.

Adrenocorticotropic Hormone↗
PubMed1987

Dog erythrocyte rosette-forming lymphocyte: blockage by OKT11 monoclonal antibody.

Human peripheral blood mononuclear cells (PBM) were separated into sheep erythrocyte rosette-forming (Es+) and non Es+ cells by the Ficoll-Hypaque gradient sedimentation method. Thirty-eight percent of the Es+ cells formed rosettes with dog erythrocytes and were designated as Es+Ed+ cells. The remaining Es+ cells were designated as Es+Ed- cells. Only a few non Es+ cells formed rosettes with dog erythrocytes. Among Es+Ed+ cells, T4 antigen-positive cells were observed approximately 1.7 times as often as T8 antigen-positive cells, when measured by staining with OKT4 or OKT8 monoclonal antibody. Among Es+Ed- cells, however, T4 and T8 antigen-positive cells were observed in almost equal proportion. Preincubation of PBM with OKT11 monoclonal antibody, but not with OKT4 monoclonal antibody, inhibited the rosette formation with dog as well as sheep erythrocytes. These results indicated that Es+Ed+ cells were a subpopulation of T-cells in which a majority of the cells were T4 antigen-positive, and that the binding sites of dog erythrocytes on human T-cells was closely linked with that of sheep erythrocytes.

Animals↗