NO alentaa inositolifosfaattien syntyä aivolisäkkeen etuosassa

Tässä otsikossa kerrotaan, että aivolisäkkeen etuosassa ( anteriorisessa hypothalamuksessa) angiotensiini II ja tyrotropiinia vapauttava hormoni stimuloivat esiin inositolifosfaattien tuotantoa. Tähän tuotantoon taas vaikuttaa typpioksidijärjestelmän signaaliaine NO tuotantoa alentavasti.

Eur J Endocrinol. 2003 Jan;148(1):89-97. Nitric oxide decreases the production of inositol phosphates stimulated by angiotensin II and thyrotropin-releasing hormone in anterior pituitary cells.

Velardez MO, Benitez AH, Cabilla JP, Bodo CC, Duvilanski BH.

Source

Centro de Investigaciones en Reproduccion, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Piso 10, Buenos Aires C1121ABG, Argentina.

Abstract (suomennosta)

OBJECTIVE:

Nitric oxide (NO) affects the synthesis of several second messengers, such as cyclic nucleotides, arachidonic acid metabolites and the intracellular calcium concentration, involved in the anterior pituitary hormone release. The present study was performed to investigate the effect of NO on phosphoinositide metabolism.

Typpioksidi(NO) vaikuttaa useitten toisiolähettien synteesiin, esim syklisten nukleotidien (cATP ym) ja arakidonihappometaboliittien synteesiin ja solunsisäiseen kalsiumin pitoisuuteen, mitkä osallistuvat aivolisäkkeen etulohkon hormonien vapautumiseen. Tämä tutkimus keskittyi nyt typpioksidin vaikutuksiin fosfoinositidin ( lipositolin, PI) aineenvaihdunnassa

METHODS:

The synthesis of inositol phosphates (IPs) was studied in primary cultures of anterior pituitary cells from Wistar male rats. IPs (mono, bis and tris phosphates) were determined by ionic exchange chromatography.

Tutkittiin IMP, IP2, IP3 inositolifosfaattimuotoa.

RESULTS:

Sodium nitroprusside and DETA NONOate (DETA/NO) significantly decreased IP synthesis and prolactin release stimulated by angiotensin II (AngII) and thyrotropin-releasing hormone (TRH). These effects were not observed with decayed DETA NONOate (unable to release NO). LY-83583, a guanylyl cyclase inhibitor, completely reversed the inhibitory effect of DETA/NO on AngII-induced IP production. However, BAY 41-2272, a novel stimulator of the soluble guanylyl cyclase, did not mimic the effect of NO donors. Likewise, neither 8-Bromine-cyclic GMP (8-Br-cGMP), an analog of cGMP, nor Sp-8-pCPT-cGMPS triethylamine, a cGMP-dependent protein kinase (PKG) stimulator, decreased IP synthesis stimulated by AngII. In addition, Rp-8-pCPT-cGMPS triethylamine, a PKG inhibitor, did not block the effect of NO. The decrease of IPs induced by DETA/NO was fully reversed by guanosine 5'-O-(3-thiotriphosphate) tetralithium salt, a non-hydrolyzable analog of GTP.

CONCLUSIONS:

The present work indicated that NO decreases IP synthesis stimulated by Ang II and TRH in anterior pituitary cells by a soluble guanylyl cyclase/cGMP/PKG-independent pathway, and suggested that NO affects some regulatory factor located between the plasma membrane receptor and G-protein.

Havaittiin, että typpioksidin NO vaikuttama ( Ang II ja TRH tekijöitten stimuloima) IP synteesin vähenemä aivolohkon etulohkossa tapahtui sellaista aineenvaihdunnallista tietä, mikä oli riippumaton sGC(cGMP(PKG-tiestä. Niinpä arvellaan että NO vaikuttaa johonkin säätelytekijään, joka sijaitsee plasmakalvoreseptorin ja G-proteiinin välissä.

PMID:

12534362

[PubMed - indexed for MEDLINE]

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