English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Cholecystokinin (CCK) is a regulatory peptide widely distributed in the body tissues and organs, that acts through two subtypes of receptors, called CCKA and CCKB, which are predominantly located in the periphery and the central nervous system, respectively. We have investigated the role of endogenous CCK in the functional regulation of the pituitaryadrenocortical axis in both normal and ether-stressed rats. To thisltask selective antagonists of CCKA and CCKB receptors (CCKA-a and CCKB-a) were administered (a single subcutaneous injection of 20 nmol/kg), and their effects on hormonal plasma concentrations were examined at various times after the injection. CCKB-a did not alter ACTH plasma concentration at 60 and 120 min in intact rats, but it raised corticosterone blood level. Conversely, CCKB-a increased ACTH plasma concentration at 60 and 120 min in ether-stressed rats, without changing the concentration of corticosterone. CCKB-a evoked a marked rise in the level of circulating ACTH in both group of rats at l5 min. CCKA-a was ineffective in both normal and stressed animals. These findings allow us to conclude that (i) endogenous CCK, acting through the CCKB receptor subtype, exerts a tonic inhibitory action on rat pituitaryadrenocortical function; and (ii) the mechanism of this action of CCK mainly involves the decrease in the pituitary ACTH release. Cholecystokinin (CCK) is a regulatory peptide involved in the regulation of satiety and stress and anxiety disorders, which is widely distributed in the central nervous system and peripheral organs and tissues. CCK exerts its biological effects through two receptor subtypes, named CCKA and CCKB, which belong to the G protein-coupled receptor superfamily and are predominantly located in the periphery and the central nervous system, respectively (for review, Correspondence to Dr Gastone G. Nussdorfer at the above address. Fax: (+39)49 827 2319, Tel: (+39)/49 827 2317, E-mail: ggnanat@ipdunidx.unipd.it. see 2). The presence of CCK and its receptors has been demonstrated in both the central and the peripheral branches of the mammalian hypothalamopituitary-adrenal (HPA) axis (for review, see 4, 6), and, accordingly, evidence is available that the systemic administration of CCK activates HPA in the rat, mainly via the CCKA receptor subtype (8, ll). Investigations dealing with the possible regulatory role played by endogenous CCK on HPA axis function are lacking. It, therefore, seemed worthwhile to explore this topic by studying the effects of selective antagonists of CCK receptors on the HPA axis of normal and stressed

Endogenous Cholecystokinin (CCK) Exerts a Tonic Inhibitory Action on Rat Pituitary-Adrenocortical Axis, Acting through the CCK-B Receptor Subtype