Nongenomic actions of steroid hormones

teroids might exert their actions by delayed genomic (classical) mechanisms, as well as by rapid, nongenomic pathways. Nongenomic action might occur in seconds or minutes. Nongenomic action includes many second messengers (inluding cAMP and diacylglycerol), kinases (mitogen-activated protein kinase, protein kinase C) and ion fluxes (calcium). The pharmacological profiles (agonist and/or antagonist selectivity) often differ markedly between the classical and nongenomic mechanisms. The identities of the receptors that are involved in nongenomic steroid actions are not yet elucidated. In some cases, classical, nuclear steroid receptors have been shown to drive signalling pathways such as kinase cascades. Gene transcription and nongenomic responses might modulate each other by crosstalk. Nongenomic steroid actions have been observed in humans (and many other vertebrates) and are probably clinically relevant. More models, such as classical-receptor knockout animals, are required to identify or rule out the receptors that are involved. Future research might widen the selection of tools, such as specific antagonists, to further explore the implications of in vivo nongenomic steroid effects and their possible therapeutic use.