摘要:

Abstract.Crude Van Dyke protein prepared from frozen bovine posterior pituitary glands was treated with formic acid to release small bound and adsorbed peptides. Gel filtration, continuous free‐flow electrophoresis and descending paper electrophoresis were used to separate the small peptides into successively purer fractions which were assayed for pressor, uterotonic, natriuretic and melanocyte stimulating activities under double blind conditions. The highest peak of natriuretic activity was associated with only a small pressor and no uterotonic activities, and the same fractions contained a ninhydrin‐positive spot on paper electrophoresis, the mobility of which at pH 5.6 was similar to that of alpha‐melanocyte stimulating hormone (MSH) and ACTH‐(1–13‐amide)‐tri‐decapeptide (1–13 ACTH‐amide) but differed from vasopressin and oxytocin. Material from this spot had an amino acid composition which corresponded with the first 13 residues of ACTH. Quantitative bioassay of the final fraction in the frog demonstrated a melanotropic activity which, however, was lower than would have been expected for pure alpha‐MSH. The natriuretic activity of the isolated fraction was far higher than the potency of separately administered peptides which might be present: arginine‐vasopressin, alpha‐MSH or 1–13 ACTH. It is suggested that the isolated fraction represents a mixture of alpha‐MSH and 1–13 ACTH, and that alpha‐MSH may be an acetylated end‐produc

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1974.tb02347.x

出版商:Blackwell Publishing Ltd    

年代:1974

数据来源: WILEY

摘要:

Abstract.Because a) a mixture of alpha‐melanotropin (MSH) and corticotropin (1–13)‐tridecapeptide (1–13 ACTH) has apparently been isolated from natriuretic fractions of posterior pituitary which also contained arginine‐vasopressin, and b) the natriuretic activity of the isolated fraction was greater than that of any of the above three peptides (synthetic) given separately, possible interaction was studied with model substances in the chloralosed cat preparation. It was found that with both alpha‐MSH and lysine‐vasopressin, extracted samples were more natriuretic than synthetic samples despite an equivalence of pressor activities. When combined with arginine‐vasopressin in one injectate, synthetic alpha‐MSH, 1–4 ACTH, 1–13 ACTH‐amide and 1–18 ACTH all showed potentiation of natriuretic activities with no effect on pressor activity. This effect was not shown by synthetic 4–10 ACTH and 5–18 ACTH, or by extracted alpha‐MSH. It was concluded that the 1–4 sequence Ser‐Tyr‐Ser‐Met, regardless of whether the N‐terminal is free or blocked, can potenti

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1974.tb02348.x

出版商:Blackwell Publishing Ltd    

年代:1974

数据来源: WILEY

摘要:

Abstract.The effect of colchicine upon glucose‐induced insulin release by the isolated perfused rat pancreas was examined in order to characterize the participation of the β‐cell microtubular apparatus in the biphasic insulin secretory response to glucose. After a short pretreatment (25 min.) with a low colchicine concentration (2.10−5M), both the early and late phases of glucose‐induced insulin secretion were markedly enhanced. As either the concentration of colchicine or the length of the pretreatment period with this mitotic spindle‐inhibitor were increased, the facilitating effect faded out and partial inhibition of insulin release was observed. However, colchicine, even at high concentration, markedly enhanced the residual early release of insulin evoked by glucose in the presence of diazoxide (0.05 mg/ml). These findings suggest that (i) a fraction of the early phase of insulin secretion completely escapes from the inhibitory effect of colchicine and may correspond, therefore, to a modality of hormonal release which does not involve the oriented intracellular translocation of secretory granules; and (ii) extensive disruption of the microtubular apparatus is associated with inhibition of insulin release, especially during the late phase of the secretory response

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1974.tb02349.x

出版商:Blackwell Publishing Ltd    

年代:1974

数据来源: WILEY

摘要:

Abstract.Colchicine failed to inhibit and actually enhanced insulin release evoked by gliclazide at a low glucose concentration (0.3 mg/ml). The facilitating action of colchicine was invariably present, whatever the concentration of (2.10−5to 10−3M) and length of exposure to (25 to 120 min.) the mitotic spindle‐inhibitor. Colchicine, and similarly cytochalasin B, also minimized the reduction in insulin output otherwise observed during the second of two successive stimulations with sulphonylurea. These data suggest that the short‐lived secretory response evoked by sulphonylurea corresponds to a modality of insulin release which does not require the oriented intracellular transport of secretory g

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1974.tb02350.x

出版商:Blackwell Publishing Ltd    

年代:1974

数据来源: WILEY

摘要:

Abstract.A model is proposed to account for the phasic nature of insulin release. It is suggested that one modality of secretion results from the mobilization of secretory granules already located in the close vicinity of the microfilamentous cell web. This corresponds to a fraction of the initial secretory response to a high glucose concentration, the residual release of insulin provoked by glucose in the presence of diazoxide, and the total release of insulin evoked by sulphonylurea at a low glucose concentration. A second modality of release, which is characteristic of the late phase of glucose‐induced insulin secretion, is thought to correspond to the mobilization of secretory granules transported to the periphery of the β‐cell along oriented microtubular pathways. Whether only one or both modalities of release are initiated by a given insulinotropic stimulus may depend on the magnitude and duration of the changes induced by secretagogues in the insular handling of cal

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1974.tb02351.x

出版商:Blackwell Publishing Ltd    

年代:1974

数据来源: WILEY

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1974.tb02352.x

出版商:Blackwell Publishing Ltd    

年代:1974

数据来源: WILEY