Modulation of the basic characteristics of cardiac activity (frequency, power of contraction, rate of conductivity and threshold of stimulation) depend on the steady but ever changing influence of two practically antagonistic nervous systems (sympathetic and parasympathetic). The mediators of the sympathetic nerve act via adrenoreceptors, the mediator of the parasympat- hetic nerve activates muscarine receptors. These type of receptors belong into the group G-protein coupled receptors. At first it seemed that in the heart are only beta1-adrenergic receptors and M2-muscarinic receptors. This idea had the advantage that both receptor systems have antagonistic effects and this antagonism is manifested most markedly on the activity of adenylate cyclase. While beta1-adrenoreceptors stimulate it, M2-muscarine receptors inhibit it. At present it is beyond doubt that adrenoreceptors are represented by sub-types alpha1, beta1, beta2. The expression of subtype beta3 known for its function in adipose tissue has not been proved unequivocally but the existence of a further, fourth type of beta-adrenoreceptors, putative beta4 seems very probable. Similarly it is certain that M 2 muscarine receptors are not the only subtype of muscarine acetylcholine receptors in cardiac tissue. The findings of new subtypes are not merely a morphological characteristics but different subtypes play a different role in the modulation of characteristics of cardiac activity, whereby a different activation, depending on the amount of mediator in their environment, is possible. Moreover receptor are not static structures but are able to change their number (and thus also the magnitude of response) and this applies to all receptor subtypes found in the heart.

        Key words: cardiac activity - receptors - sympathetic nerve - parasympathetic nerve - G-protein