-adrenoceptor regulation in the human heart: can it be monitored in circulating lymphocytes?

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Abstract
In heart failure a decrease in cardiac β-adrenoceptors presumably due to endogenous down-regulation by the elevated catecholamines is a general phenomenon. Thus, attempts have been made to assess β-adrenoceptor function in patients with chronic heart failure in order to monitor the functional state of cardiac β-adrenoceptors. The model most widely used is that of circulating lymphocytes that contain a homogeneous population of β2-adrenoceptors coupled to the adenylate cyclaselcyclic AMP system. The biochemical and pharmacological properties of β2-adrenoceptors present in lymphocytes are quite comparable to those of β2-adrenoceptors in the human heart, but clearly different from those of human cardiac β1-adrenoceptors. Furthermore, β-adrenoceptor agonists and antagonists regulate lymphocyte β2- and cardiac β1- and β2-adrenoceptors in a subtype-selective fashion: while non-selective agonists (independent of exogenously applied or endogenously elevated) and antagonists affect both cardiac β1- and β1- as well as lymphocyte β2-adrenoceptors, β1-selective agonists and antagonists influence only cardiac β1-, but not cardiac and lymphocyte β2-adrenoceptors. Finally, direct comparison of lymphocyte and cardiac β-adrenoceptor densities revealed that changes in lymphocyte β2-adrenoceptors are significantly correlated with changes in cardiac β2-adrenoceptors, but not related to changes in cardiac β1-adrenoceptors. Since β1-adrenoceptors predominate in all parts of the human heart, the use of lymphocyte β2-adrenoceptors as a tool for predicting the status of cardiac β-adrenoceptors is, therefore, quite limited.

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