Detail of "73168-24-8"

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Stimulation of adrenocorticotropin/b-endorphin release by synthetic ovine corticotropin-releasing factor in vitro

Stimulation of adrenocorticotropin/b-endorphin release by synthetic ovine corticotropin-releasing factor in vitro. Enhancement by various vasopressin analogs. Knepel, Willhart; Homolka, Lutz; Vlaskovska, Mila; Nutto, Doris (Univ. Freiburg/Br., Freiburg/Br. D-7800, Fed. Rep. Ger.). Neuroendocrinology, 38(5), 344-50 (English) 1984. CODEN: NUNDAJ. ISSN: 0028-3835. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The ability of vasopressin analogs to enhance the release of ACTH [9002-60-2] immunoreactivity (ACTH-IR) and b-endorphin [60617-12-1]-like immunoreactivity (b-EI) induced by synthetic ovine CRF (CRF-(1-41)) [79804-71-0] was studied in vitro with incubated rat anterior pituitary quarters. Arginine vasopressin (AVP) [113-79-1] potentiated the action of CRF-(1-41) 2-4-fold. Vasopressin analogs, which possess direct CRF-like activity when given alone, also enhanced b-EI release caused by CRF-(1-41); the lowest concn. able to potentiate CRF-(1-41) activity was closely correlated with the ED50 value of these analogs for direct CRF-like activity. [1-(b-Mercapto-b,b-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine, 8-arginine]vasopressin [73168-24-8] blocked the release of ACTH-IR induced by AVP; however, this analog failed to prevent the potentiation by AVP of ACTH-IR release caused by CRF-(1-41), but it enhanced the action of CRF-(1-41). Two analogs, which exhibited no direct CRF-like activity and which also did not antagonize the CRF-like activity of AVP, markedly enhanced the ACTH-IR and b-EI response to CRF-(1-41). These data indicate that the potency of vasopressin analogs for enhancing the action of CRF-(1-41) is not related to their reported vasopressor or antidiuretic activity and provide some evidence that the structural requirements for potentiation by vasopressin of CRF-(1-41) action may be different also from those parts of the vasopressin mol. which confer the ability to induce ACTH-IR/b-EI release in the absence of CRF-(1-41).

Evidence that the effects of arginine-8-vasopressin (AVP) on pituitary corticotropin (ACTH) release are mediated by a novel type of receptor

Evidence that the effects of arginine-8-vasopressin (AVP) on pituitary corticotropin (ACTH) release are mediated by a novel type of receptor. Antoni, Ferenc A.; Holmes, Megan C.; Makara, Gabor B.; Karteszi, Mihaly; Laszlo, Ferenc A. (Inst. Exp. Med., Hung. Acad. Sci., Budapest, Hung.). Peptides (Fayetteville, N. Y.), 5(3), 519-22 (English) 1984. CODEN: PPTDD5. ISSN: 0196-9781. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Whether the effect of arginine vasopressin (AVP) [113-79-1], either in the presence or in the absence of ovine corticotropin-releasing factor (oCRF-41) [9015-71-8] (0.5 nmol/L), was blocked by V1 (pressor)-antagonists was examd. Oxytocin [50-56-6], and [1-deamino,8-D-arginine] vasopressin (dDAVP) [16679-58-6] were also tested for their ability to release ACTH [9002-60-2]. All expts. were carried out in vitro, using segments of rat anterior pituitary glands. The V1-antagonist [1-deamino,penicillamine(O-methyl-tyrosine)]AVP [67269-08-3] inhibited ACTH release induced by AVP or AVP + oCRF-41. However, it also had some agonistic activity which was more pronounced in the presence of oCRF-41. An equally potent V1-antagonist, [1-b-mercapto-b,b-cyclopentamethyleneproprionic acid (O-methyl-tyrosine)]AVP [73168-24-8], failed to inhibit AVP-stimulated ACTH secretion, and also had weak agonist potency. The relatively selective V2 (antidiuretic)-agonist dDAVP was 20-30-fold less potent than AVP. Oxytocin, a weak V1- and V2-agonist was only 4-8-fold less potent than AVP. Apparently AVP receptors on pituitary corticotroph cells are neither classical V1- nor V2-receptors.