-adrenoceptor density and relative number of  -adrenoceptor subtypes in biopsies from human right atrial, left ventricular, and right ventricular myocard

Abstract

In the present study we estimated the relative number of beta-adrenoceptors in membrane preparations from right atrial and left ventricular biopsies from 8 patients, as well as from right ventricular biopsy from one patient. Determinations of relative number of beta adrenoceptor subtypes (beta1, beta2) were also performed. Estimations were performed in a radioligand assay, measuring specific binding of [125I]-cyanopindolol (CYP). Inhibition of specific [125I] CYP binding was studied by adding propranolol (non-selective antagonist), atenolol (beta1 selective antagonist) and ICI 118551 (beta2 selective antagonist) to the preparations. Some individual variance in total number of receptors was found. Per mg protein, the number of binding sites were higher in atrial preparations (mean 71.4 +/- 14.4 fmol X mg-1) than in left ventricular preparations (mean 30.2 +/- 7.1 fmol X mg-1). Receptor number in the right ventricular preparation was 49.5 +/- 2.6 fmol X mg-1. Approximately 25% of beta adrenoceptors were of beta2 subtype in preparations from both right atrial and left ventricular biopsies, as well as from the right ventricular biopsy. Thus, there are regional differences in the quantity of beta adrenoceptors in human myocard whereas the relative proportion of beta1 and beta2 receptors appears to be fairly constant.

Characterization and autoradiographic localization of β‐adrenoceptor subtypes in human cardiac tissues

“…The affinity of the ligand for P-adrenoceptors in the slidemounted sections was similar to that found in homogenate binding studies ofhuman atria (Brodde et al, 1983;Heitz et al, 1983;Robberecht et al, 1983;Stiles et al, 1983;Golf et al, 1985;Hedberg et al, 1985) and cardiac P-adrenoceptors of other animal species (McPherson et al, 1984). The receptor density (Bmax) was also similar in sections and in some homogenate binding studies of human atria (Robberecht et al, 1983;Stiles et al, 1983;Golf et al, 1985;Hedberg et al, 1985), yet half that found in other studies (Brodde et al, 1983;Hedberg et al, 1985).…”

“…The percentage of P2-adrenoceptors in atrial sections was higher than that in some studies (20-26%) (Brodde et al, 1983;Heitz et al, 1983;Stiles et al, 1983;Golf et al, 1985) but less than that in others (50-55%) (Robberecht et al, 1983;Hedberg et al, 1985).…”

“…In man, 20-50% of the P-adrenoceptors are of the p2-subtype in right atrial appendage (Brodde et al, 1983;Heitz et al, 1983;Robberecht et al, 1983;Stiles et al, 1983;Golf et al, 1985;Hedberg et al, 1985) and 14 -36% in left ventricle (Heitz et al, 1983;Stiles et al, 1983;Vago et al, 1984;Golf et al, 1985). In these studies utilizing homogenates the true myocardial P2-adrenoceptor concentration is unknown because of ) The Macmillan Press Ltd 1987 the contribution of P2-adrenoceptors from other cells such as fibroblasts (Lau et al, 1980), nerves (Rand et al, 1980;Lipe & Summers, 1986; and on the endothelium ofblood vessels (Lipe & Summers, 1986;Stephenson & Summers, 1987).…”

Amiodarone-Induced Thyroid Dysfunction and Ventricular Tachyarrhythmias During Long-Term Therapy in Japan.

“…Patients with hyperthyroidism often develop atrial arrhythmias because the atria are more sensitive than the ventricles to the effect of thyroid hormones. 9,10 This preferential atrial arrhythmogenic effect of thyroid hormones seems to be caused by various factors such as atrialadrenergic receptor density 11 or differences between atrial and ventricular autonomic innervation and differences in sensitivity. 4 However, hyperthyroidism associated with organic heart disease or marked heart failure can cause malignant arrhythmias, including ventricular tachycardia and fibrillation.…”

Reentrant Atrioventricular Nodal Tachycardia Induced by Levothyroxine

“…The molecular cloning of an individual cardiac ion channel has provided important new information on the molecular basis of cardiac excitability. The preferential atrial arrhythmogenic effect of thyroid hormones could also be caused by the increased atrial ␤-adrenergic receptor density (14) in the presence of reduced parasympathetic tone (15,16). Thus, it is conceivable that ␤-adrenergic blockade might reduce the arrhythmogenic effect of thyroid hormone in patients predisposed to supraventricular tachycardia, when L-T 4 treatment is considered indispensable.…”