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001-es BibID:	BIBFORM059641
035-os BibID:	(WOS)000357682500005 (Scopus)84937515738
Első szerző:	Pák Krisztián (gyógyszerész)
Cím:	The effect of adenosine deaminase inhibition on the A1 adenosinergic and M2 muscarinergic control of contractility in eu- and hyperthyroid guinea pig atria / Krisztian Pak, Judit Zsuga, Zita Kepes, Tamas Erdei, Balazs Varga, Bela Juhasz, Andras Jozsef Szentmiklosi, Rudolf Gesztelyi
Dátum:	2015
Megjegyzések:	The A1 adenosine and M2 muscarinic receptors exert protective (including energy consumption limiting) effectsin the heart.We investigated the influence of adenosine deaminase (ADA) inhibition on a representative energy consumption limiting function, the direct negative inotropic effect elicited by the A1 adenosinergic and M2 muscarinergic systems, in eu- and hyperthyroid atria. Furthermore, we compared the change in the interstitial adenosine level caused by ADA inhibition and nucleoside transport blockade, two well-established processes to stimulate the cell surface A1 adenosine receptors, in both thyroid states. A classical isolated organ technique was applied supplemented with the receptorial responsiveness method (RRM), a concentration estimating procedure. Via measuring the contractile force, the direct negative inotropic capacity of N6-cyclopentyladenosine, a selectiveA1 receptor agonist, and methacholine, a muscarinic receptoragonist, was determined on the left atria isolated from 8-day solvent- and thyroxine-treated guinea pigs in the presence and absence of 2·-deoxycoformycin, a selectiveADA inhibitor, and NBTI, a selective nucleoside transporter inhibitor. We found that ADA inhibition (but not nucleoside transport blockade) increased the signal amplification of the A1 adenosinergic (but not M2 muscarinergic) system. This action of ADA inhibition developed in both thyroid states, but it was greater in hyperthyroidism. Nevertheless, ADA inhibition produced a smaller rise in the interstitial adenosine concentration than nucleoside transport blockade did in both thyroid states. Our results indicate that ADA inhibition, besides increasing the interstitial adenosine level, intensifies the atrialA1 adenosinergic function in another (thyroid hormonesensitive) way, suggesting a new mechanism of action of ADA inhibition.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Adenosine deaminase inhibition Thyroid hormones Heart Atrium Guinea pig RRM
Megjelenés:	Naunyn-Schmiedeberg's archives of pharmacology. - 388 : 8 (2015), p. 853-868. -
További szerzők:	Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Képes Zita (1991-) (orvos) Erdei Tamás Dániel (1992-) (kísérletes farmakológus) Varga Balázs (1984-) (kísérletes farmakológus) Juhász Béla (1978-) (kísérletes farmakológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Gesztelyi Rudolf (1969-) (kísérletes farmakológus)
Pályázati támogatás:	TÁMOP-4.2.4.A/2-11-1-2012-0001 TÁMOP TÁMOP-4.2.2.A-11/1/KONV-2012-0045 TÁMOP
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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