title: Comparison of the effect of left ventricular volume and pressure overload on beta-adrenoceptor density in left heart valvular disease.
abstract: The sympathetic responses in left heart valvular disease may depend on the ventricular load conditions. We proposed to evaluate this possibility by comparing the effects of left ventricular pressure (LVP) and volume (LVV) overload on beta-adrenoceptor density and ligand binding affinity in lymphocytes and in the four myocardial chambers in rheumatic heart valvular patients. Receptor activity was determined by radioligand binding using [125I]iodocyanopindolol. In the lymphocytes (n = 45), the beta-adrenoceptor density was reduced by 88% (P < 0.001) in LVP patients (n = 15) and 79% (P < 0.001) in LVV patients (n = 30) compared with 23 controls. In the myocardium, the receptor density of the LVP (n = 12) was attenuated by 55% (P < 0.05) in the left ventricle, 42% in the right ventricle, 13% in the left atrium, and 37% in the right atrium, while in LVV patients (n = 22) it decreased by 73% (P < 0.01) in the left ventricle, 62% (P < 0.05) in the right ventricle, 30% in the left atrium, and 34% in the right atrium compared with 15 controls. Thus, the reduction in density was greatest in lymphocytes and least in the atria in both groups. The decrease in ventricular density of the LVV group was similar to the reduction in the lymphocytes and two-fold higher than in the atrial density. These alterations were significantly greater for the LVV than for the LVP group. The Kd for the myocardial receptor binding to [125I]iodocyanopindolol was not significantly influenced in either group, but was lower in the lymphocytes. These findings suggest that in patients with left heart valvular disease, there is a significant attenuation in both peripheral and myocardial beta-adrenoceptor density. The decrease in receptor density is significantly greater in the left ventricular volume overload than in the left ventricular pressure overload patients.
authors.affiliation: Biological and Medical Research Department, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
authors.forename: N
authors.initials: N
authors.lastname: Dzimiri
authors.forename: A
authors.initials: A
authors.lastname: Moorji
authors.forename: M
authors.initials: M
authors.lastname: Kumar
authors.forename: N
authors.initials: N
authors.lastname: Kumar
authors.forename: Z
authors.initials: Z
authors.lastname: Halees
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001022:Aortic Valve Insufficiency / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D001024:Aortic Valve Stenosis / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D002306:Cardiac Volume / Q000502:physiology; D005260:Female; D006350:Heart Valve Prosthesis; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D009206:Myocardium / Q000473:pathology; D011869:Radioligand Assay; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D012016:Reference Values; D012214:Rheumatic Heart Disease / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D013318:Stroke Volume / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D011943:Receptors, Adrenergic, beta