Summary
In the common unidimensional theory of steroid action, steroids bind to intracellular
receptors and modulate nuclear transcription and thus protein synthesis. These genomic
steroid effects, being characterized by their delayed onset of action and their dependence
on transcription and protein synthesis, have been known for several decades. In contrast,
very rapid actions of steroids, which are considered to be of nongenomic origin, have
been recognized more widely and characterized in detail only during the past ten years.
Specific rapid effects of steroids and related hormones like vitamin D3 and thyroid
hormones on cellular function involve a conventional second messenger cascade which
in most cases includes phospholipase C, phosphoinositide turnover, intracellular pH
and intracellular calcium ([Ca2+]i), and protein kinase C. Furthermore, binding sites in membranes have been characterized
exposing binding features compatible with an involvement in rapid-steroid signaling.
Characteristics of putative membrane receptors are completely different from those
of classic intracellular steroid receptors; this also includes the inability of classic
steroid receptor antagonists to inhibit those rapid nongenomic steroid actions.
The physiological and pathophysiological relevance of these effects is still largely
unclear, but their existence has been proven recently even under in vivo conditions.
New drugs modulating nongenomic steroid actions may find applications in various areas
such as the cardiovascular and central nervous systems, infertility and electrolyte
homeostasis.
This short review focuses mainly on the nongenomic actions of aldosterone and their
cardiovascular implications.
Key words
Aldosterone - steroids - nongenomic action - membrane receptors - second messengers
