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Effect of metoprolol on activity of beta-adrenoceptor coupled to guanine nucleotide binding regulatory proteins in adriamycin-induced cardiotoxicity.

Artikel i vetenskaplig tidskrift
Författare Michael Fu
Claes-Håkan Bergh
Johan Hoebeke
Qi-Ming Liang
Klas-Göran Sjögren
Finn Waagstein
Åke Hjalmarson
Publicerad i Basic research in cardiology
Volym 86
Nummer/häfte 2
Sidor 117-26
ISSN 0300-8428
Publiceringsår 1991
Publicerad vid Wallenberglaboratoriet
Hjärt-kärlinstitutionen
Sidor 117-26
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adenylate Cyclase, metabolism, Animals, Blotting, Northern, Calcium-Transporting ATPases, metabolism, Doxorubicin, GTP-Binding Proteins, genetics, metabolism, Heart Diseases, chemically induced, metabolism, Iodine Radioisotopes, diagnostic use, Iodocyanopindolol, Kinetics, Male, Membranes, metabolism, Metoprolol, pharmacology, Nucleic Acid Hybridization, Pindolol, analogs & derivatives, diagnostic use, RNA, Messenger, metabolism, Radioligand Assay, Rats, Rats, Inbred Strains, Receptors, Adrenergic, beta, drug effects
Ämneskategorier Fysiologi

Sammanfattning

Prevention of cardiotoxicity without interfering with the therapeutic efficacy of adriamycin is a very crucial question. We have investigated the activity of beta-adrenoceptor coupled to guanine nucleotide binding regulatory proteins (G-proteins) and Ca(2+)-ATPase activity in experimental adriamycin-induced cardiotoxicity and the influence of metoprolol treatment on these variables. Adriamycin was administered to rats intravenously as a single dose of 6 mg/kg, and metoprol was continuously given by means of implanted osmotic pumps. beta-Adrenoceptor characteristics were measured by radioligand-binding experiments and by basal and stimulated adenylyl cyclase activity. Northern blot and dot blot analysis was used to quantify G-protein mRNA. It was shown that adriamycin did not induce any change in the total beta-adrenoceptor density, nor did the high affinity agonist binding to beta-adrenoceptor change. Adriamycin did not induce any alteration in the amount of mRNA encoding for stimulatory (Gs) or inhibitory (Gi) G-proteins. Also, basal and stimulated adenylyl cyclase activities were identical in the different experimental groups. In contrast, the Ca(2+)-ATPase was shown to increase in adriamycin-treated rats compared to control rats (45 +/- 3.8 versus 23 +/- 1.2 mumol Pi/mg/h, P less than .01). Metoprolol was shown to normalize this increase (29 +/- 2.1 mumol Pi/mg/h). Thus, it may be concluded that in experimental adriamycin-induced cardiotoxicity, despite Ca(2+)-overloading, the beta-adrenoceptor-G protein-adenylyl cyclase system remains intact. Metoprolol seems to prevent Ca(2+)-overloading independently of the beta-adrenoceptors studied here.

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