| Popis: |
The current knowledge on the cellular signal transformations by subtypes of adrenergic receptors is presented. Stimulation of either β-adrenergic receptor, i.e., β1 or β2, causes an increase in the cellular concentration of cyclic AMP via stimulation of the adenylate cyclase. An opposite change in the cellular cyclic AMP concentration via inhibition of the adenylate cyclase appears to be the first intracellular signal caused by stimulation of α2-adrenergic receptors. The coupling of β-adrenergic receptors to adenylate cyclase is mediated by a regulatory guanyl nucleotide-binding protein, whose interactions with the receptor and the enzyme are relatively well characterized. The molecular mechanisms of the α2-adrenergic signal transformation, which also appears to be mediated by a guanyl nucleotide-binding component, are less clear and may involve an accelerated inactivation of the adenylate cyclase by an increased GTPase activity. Stimulation of α1-adrenergic receptors causes several changes possibly involved in the final cellular response. Among these, the increase in the cytoplasmic calcium concentration is the most important signal, which may be triggered by an increased membrane phosphatidylinositol turnover, while the increase in cellular cyclic GMP levels appears to be a consequence of the increased calcium concentration and other cellular changes yet not fully understood. The relevance of these three main cellular signal-generating systems for the cellular regulation via other than adrenergic hormone and neurotransmitter receptors and receptor subtypes is discussed. |
