Characterization of lymphocyte β‐adrenoceptor activity and Gs‐protein in patients with rheumatic heart valvular disease
Identifieur interne : 002B78 ( Main/Exploration ); précédent : 002B77; suivant : 002B79Characterization of lymphocyte β‐adrenoceptor activity and Gs‐protein in patients with rheumatic heart valvular disease
Auteurs : N. Dzimiri ; S. Hussain ; A. Moorji ; G. Prabhakar ; S. Bakr ; M. Kumar ; Aa Almotrefi [Arabie saoudite] ; Z. HaleesSource :
- Fundamental & Clinical Pharmacology [ 0767-3981 ] ; 1995-07-08.
English descriptors
- Teeft :
- Adenylate, Adenylate cyclase, Adrenergic, Aortic, Binding affinity, Binding sites, Bristow, Brodde, Camp levels, Catecholamine, Codon, Control group, Cyclase, Dzimiri, Ejection fractions, Epinephrine, Exon, Heart failure, Human heart, Lesion, Lymphocyte, Mitral, Mitral stenosis, Mutation, Mutational changes, Norepinephrine, Nyha, Nyha class, Other hand, Overload, Padrenergic, Padrenoceptor, Padrenoceptor activity, Padrenoceptor density, Padrenoceptors, Plasma catecholamine, Plasma norepinephrine, Present study, Pressure overload, Protein activity, Receptor, Receptor density, Rheumatic, Rheumatic heart valvular disease, Rheumatic valvular disease, Significant difference, Stenosis, Study population, Valvular, Valvular diseases, Ventricular, Ventricular load conditions, Ventricular pressure overload, Ventricular volume overload, Volume overload.
Abstract
Summary— In order to test whether the β‐adrenoceptor activity in rheumatic heart valvular disease depends on the ventricular load conditions, we determined their density and binding affinity to [125I]‐iodocyanopindolol in lymphocytes, as well as plasma catecholamine and cAMP levels in 69 patients with regurgitant and stenotic lesions of the aortic and mitral valves. The patients were classified as having left ventricular pressure overload (LVP), left ventricular volume overload (LVV), mixed lesions (MOL) or right ventricular pressure overload (RVP). The β‐adrenoceptor activity was determined by radioligand binding methods, catecholamines by high performance liquid chromatography using an electrochemical detector and cAMP by radioimmunoassay. The mean β‐adrenoceptor density (Bmax) of the control group was 60.1 ± 9.5 /mol (n = 29) per 106 lymphocytes. In the study population, the density was decreased by 83% in LVP, 78% in LVV, 87% in MOL and 86% in RVP. Plasma norepinephrine was elevated by 89% in LVP and 60% in MOL, epinephrine by 43% in LVP, 50% in VOL, 115% in MOL and 20% in RVP, while dopamine was not significantly changed, and cAMP was slightly elevated in all four groups. Screening for activating mutational changes in the Gsα‐protein gave negative results, possibly dissociating the elevation in plasma cAMP from stimulatory effects of such abnormalities in the Gs‐protein signaling. These results show a significant attenuation in lymphocyte β‐adrenoceptor density of patients with rheumatic heart valvular disease, irrespective of the type of the prevailing ventricular load conditions. The reduction in receptor density is accompanied by a significant increase in plasma norepinephrine levels in patients with a left ventricular pressure overload and epinephrine in those with volume overload.
Url:
DOI: 10.1111/j.1472-8206.1995.tb00512.x
Affiliations:
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The patients were classified as having left ventricular pressure overload (LVP), left ventricular volume overload (LVV), mixed lesions (MOL) or right ventricular pressure overload (RVP). The β‐adrenoceptor activity was determined by radioligand binding methods, catecholamines by high performance liquid chromatography using an electrochemical detector and cAMP by radioimmunoassay. The mean β‐adrenoceptor density (Bmax) of the control group was 60.1 ± 9.5 /mol (n = 29) per 106 lymphocytes. In the study population, the density was decreased by 83% in LVP, 78% in LVV, 87% in MOL and 86% in RVP. Plasma norepinephrine was elevated by 89% in LVP and 60% in MOL, epinephrine by 43% in LVP, 50% in VOL, 115% in MOL and 20% in RVP, while dopamine was not significantly changed, and cAMP was slightly elevated in all four groups. Screening for activating mutational changes in the Gsα‐protein gave negative results, possibly dissociating the elevation in plasma cAMP from stimulatory effects of such abnormalities in the Gs‐protein signaling. These results show a significant attenuation in lymphocyte β‐adrenoceptor density of patients with rheumatic heart valvular disease, irrespective of the type of the prevailing ventricular load conditions. The reduction in receptor density is accompanied by a significant increase in plasma norepinephrine levels in patients with a left ventricular pressure overload and epinephrine in those with volume overload.</div></front></TEI><affiliations><list><country><li>Arabie saoudite</li></country></list><tree><noCountry><name sortKey="Bakr, S" sort="Bakr, S" uniqKey="Bakr S" first="S." last="Bakr">S. Bakr</name><name sortKey="Dzimiri, N" sort="Dzimiri, N" uniqKey="Dzimiri N" first="N." last="Dzimiri">N. Dzimiri</name><name sortKey="Halees, Z" sort="Halees, Z" uniqKey="Halees Z" first="Z." last="Halees">Z. Halees</name><name sortKey="Hussain, S" sort="Hussain, S" uniqKey="Hussain S" first="S." last="Hussain">S. Hussain</name><name sortKey="Kumar, M" sort="Kumar, M" uniqKey="Kumar M" first="M." last="Kumar">M. Kumar</name><name sortKey="Moorji, A" sort="Moorji, A" uniqKey="Moorji A" first="A." last="Moorji">A. Moorji</name><name sortKey="Prabhakar, G" sort="Prabhakar, G" uniqKey="Prabhakar G" first="G." last="Prabhakar">G. Prabhakar</name></noCountry><country name="Arabie saoudite"><noRegion><name sortKey="Almotrefi, Aa" sort="Almotrefi, Aa" uniqKey="Almotrefi A" first="Aa" last="Almotrefi">Aa Almotrefi</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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