摘要:

In this study we investigated in the rat the binding and corticotropin-releasing factor (CRF) activity of various constituents of the renin-angiotensin system and the possible angiotensin II receptor changes following procedures known to alter plasma renin activity. We investigated also the CRF activity of angiotensin II in vitro and in vivo in humans. The CRF activity of peptides was studied by their ability to stimulate ACTH release from pituitary cells. Deleting amino acids from the N-terminus of angiotensin II resulted in decreased CRF activity; while the ED50 for angiotensin II was 2 nM, it increased to about 10 nM for the (2–8)-heptapeptide. Angiotensin I had a weak CRF activity, whereas the substrate angiotensinogen had no stimulatory effect even at a concentration of 100 nM. There was a strong correlation between the activation and binding properties of all peptides tested. Dietary salt load or depletion as well as dexamethasone treatment did not affect the number nor the affinity of pituitary angiotensin II receptors. Angiotensin II had a CRF activity on human pituitary cells in vitro. However, peripherally injected agiotensin II at a pressive dose of 7 ng/kg/min did not produce any ACTH release in normal male volunteers. These data suggest that angiotensin II may play a modulatory role in the physiological regulation of ACTH secretion, but this role might be attributed to the endogenous brain angiotensin II as it is not closely dependent on the angiotensin II plasma level

ISSN:0028-3835    

DOI:10.1159/000124228

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

To ascertain the physiological relevance of an autoregulation of adrenocorticotropic hormone (ACTH) secretion in man, we studied the effect of alsactide (β-Alai, Lys17-ACTH1-17-4-amino-N-butylamide), a synthetic ACTH analogue with potent steroidogenic activity but not recognized in the endogenous ACTH immunoassay, on plasma ACTH pattern in patients with Addison’s disease. Three experimental models were employed as follows: (a) in 6 patients, whose steroid replacement therapy had been discontinued 36 h previously, we compared the effect of alsactide, administered at two dose levels (10 or 100 µg i.v. as bolus followed by the same dose infused over 2 h, and of placebo, on the plasma ACTH pattern; (b) the previous experiment was repeated in 4 patients in whom cortone replacement therapy was substituted for 3 days with dexamethasone, 0.5–1.5 mg daily p.o., so as to lower plasma ACTH levels to within the high normal range; (c) in 4 patients off therapy for 36 h, we evaluated the ACTH response to synthetic ovine corticotropin-releasing factor, 1 µg/kg body weight injected intravenously, occurring during concomitant administration of alsactide, 100 µg i.v. as bolus plus 100 µg infused over 2 h, or placebo. Compared to placebo, alsactide did not significantly affect the pattern of ACTH under any of the experimental conditions investigated. Collectively, our findings, although they have to be interpreted with caution, do not support the idea that a self-regulation mechanism plays an important role in the control of ACTH secretio

ISSN:0028-3835    

DOI:10.1159/000124229

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

We have previously described the presence and wide distribution of a luteinizing hormone (LH)-like peptide, widely distributed in the rat central nervous system, with highest levels in the hypothalamus. We have found that intracerebroventricular injection of 100 µg colchicine causes a significant rise in hypothalamic LH, from 549 ± 170 pg/mg protein (n = 12) in controls to 1,679 ± 279 pg/mg protein (n = 13) in treated animals, p < 0.01. There was no associated change in levels of LH in the pituitary. Since colchicine stops axoplasmic flow, these findings of colchicine-induced increase in hypothalamic LH indicate that at least a portion of hypothalamic LH is present in long-axoned neuronal elements with cell bodies within the hypothalamus and axons extending to the extrahypothalamic brain. Thus, hypothalamic LH does not solely represent measurement of LH in cells of the contignous pars tuberal

ISSN:0028-3835    

DOI:10.1159/000124230

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effect of immunoneutralization of endogenous vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI)-like peptides by administration of specific and potent antisera to the respective peptides on ether stress-induced prolactin (PRL) release was examined in male rats bearing an indwelling atrial catheter. Forty-five minutes after an injection of 1 ml of either normal rabbit serum (NRS), anti-VIP serum (AVS), anti-PHI serum (APS) or AVS plus APS, the rat was placed for 1 min in a beaker containing an ether-impregnated cotton ball. Ether exposure caused a prompt and significant increase in plasma PRL in all of the animal groups tested. Pretreatment with either antisera did not affect basal plasma PRL levels, whereas plasma PRL rises after ether exposure were significantly lower in rats pretreated with AVS, APS or AVS plus APS than those with NRS. These results suggest that hypothalamic VIP and PHI-like peptides may be involved, at least in part, in the mechanism by which ether stress stimulates PRL secretion in rats.

ISSN:0028-3835    

DOI:10.1159/000124231

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124233

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124234

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124235

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124217

出版商:S. Karger AG    

年代:1985

数据来源: Karger