scholarly journals Purification of Dipeptidyl Aminopeptidase II (Dipeptidyl Arylamidase II) of the Anterior Pituitary Gland

1968 ◽  
Vol 243 (15) ◽  
pp. 4143-4150 ◽  
Author(s):  
J K McDonald ◽  
F H Leibach ◽  
R E Grindeland ◽  
S Ellis
1979 ◽  
Vol 16 (2) ◽  
pp. 99-112 ◽  
Author(s):  
Thérèse Di Paolo ◽  
Réjean Carmichael ◽  
Fernand Labrie ◽  
Jean-Pierre Raynaud

1984 ◽  
Vol 100 (2) ◽  
pp. 219-226 ◽  
Author(s):  
S. A. Nicholson ◽  
T. E. Adrian ◽  
B. Gillham ◽  
M. T. Jones ◽  
S. R. Bloom

ABSTRACT The effect of six hypothalamic peptides on the basal release of ACTH and that induced by arginine vasopressin (AVP) or by ovine corticotrophin releasing factor (oCRF) from fragments of the rat anterior pituitary gland incubated in vitro was investigated. Dose–response curves to AVP and to oCRF were obtained, and the response to a low dose of oCRF was potentiated by a low dose of AVP. Basal release of ACTH was not affected by any of the peptides in concentrations in the range 10−12 to 10−6 mol/l, and only substance P (SP) and somatostatin (SRIF) inhibited significantly the response to oCRF in a dose-related manner. The responses to a range of doses of oCRF or AVP were reduced by 10−8 and 10 − 6 mol SP or SRIF/1, and to a greater extent by the higher dose. Except in the case of 10−6 mol SRIF/1 on the response to AVP, the response was not further diminished by preincubation of the tissue with the peptide before the stimulating agent was added. The inhibition of the responses to AVP or oCRF by 10−9 mol SP/1 was not potentiated by its combination with either 5 × 10−10 or 10−8 mol SRIF/1; the inhibitory effects were merely additive. The results suggest that although SRIF and SP are able to modulate the release of ACTH from the anterior pituitary gland, they do so only at a high concentration. In the case of SRIF these concentrations are several orders of magnitude higher than those reported to be present in the hypophysial portal blood and therefore a physiological role for this peptide in the control of ACTH secretion is unlikely. J. Endocr. (1984) 100, 219–226


1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.


2014 ◽  
Vol 357 (1) ◽  
pp. 301-308 ◽  
Author(s):  
Kotaro Horiguchi ◽  
Ken Fujiwara ◽  
Saishu Yoshida ◽  
Masashi Higuchi ◽  
Takehiro Tsukada ◽  
...  

BioScience ◽  
1979 ◽  
Vol 29 (7) ◽  
pp. 408-413 ◽  
Author(s):  
Edward G. Rennels ◽  
Damon C. Herbert

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