Cardiac effects of β-adrenergic blockers in combination with metabolic interventions

Abstract

It is well known that catecholamines have pronounced hemodynamic and metabolic effects. As shown in Fig. 1, catecholamines interact with the s-receptor of the myocardial cell and stimulate via a GTP-binding protein adenylate cyclase (1). The resulting increase in cAMP (2) activates protein kinases that are involved in different metabolic and functional processes. Apart from stimulating lipolysis mainly in organs other than the heart, there is an increase in glycogenolysis. Phosphorylation appears to be also involved in the initiation of functional effects. In this way, the Ca++ influx through the sarcolemma (3,4) becomes enhanced and thus the increased contractility is brought about. On the other hand, troponin I (5) and phospholamban are phosphorylated (6), the latter resulting in an increased uptake of Ca++ into the sarcoplasmic reticulum and in the acceleration of relaxation. Catecholamines also influence glycolysis and the pentose phosphate pathway (7,8) and, as a consequence of this, the de novo synthesis of adenine nucleotides (9) and ultimately RNA and protein synthesis (10).