Steroid hormones modulate many physiological processes. The effects of steroids that are mediated by the modulation of gene expression are known to occur with a time lag of hours or even days. Research that has been carried out mainly in the past decade has identified other responses to steroids that are much more rapid and take place in seconds or minutes. These responses follow nongenomic pathways, and they are not rare.

https://www.auburn.edu/academic/classes/biol/6190/refs/L06/8818952.pdf

Nongenomic actions of steroid hormones

The adrenal hormone corticosterone transcriptionally regulates responsive genes in the rodent hippocampus through nuclear mineralocorticoid and glucocorticoid receptors. Via this genomic pathway the hormone alters properties of hippocampal cells slowly and for a prolonged period. Here we report that corticosterone also rapidly and reversibly changes hippocampal signaling. Stress levels of the hormone enhance the frequency of miniature excitatory postsynaptic potentials in CA1 pyramidal neurons and reduce paired-pulse facilitation, pointing to a hormone-dependent enhancement of glutamate-release probability. The rapid effect by corticosterone is accomplished through a nongenomic pathway involving membrane-located receptors. Unexpectedly, the rapid effect critically depends on the classical mineralocorticoid receptor, as evidenced by the effectiveness of agonists, antagonists, and brain-specific inactivation of the mineralocorticoid but not the glucocorticoid receptor gene. Rapid actions by corticosterone would allow the brain to change its function within minutes after stress-induced elevations of corticosteroid levels, in addition to responding later through gene-mediated signaling pathways.

https://www.pnas.org/content/pnas/102/52/19204.full.pdf

Mineralocorticoid receptors are indispensable for nongenomic modulation of hippocampal glutamate transmission by corticosterone

The function of the pancreatic β-cell is the storage and release of insulin, the main hormone involved in blood glucose homeostasis. The results in this article show that the widespread environmental contaminant bisphenol-A (BPA) imitates 17β-estradiol (E2) effects in vivo on blood glucose homeostasis through genomic and nongenomic pathways. The exposure of adult mice to a single low dose (10 μg/kg) of either E2 or BPA induces a rapid decrease in glycemia that correlates with a rise of plasma insulin. Longer exposures to E2 and BPA induce an increase in pancreatic β-cell insulin content in an estrogen-receptor–dependent manner. This effect is visible after 2 days of treatment and starting at doses as low as 10 μg/kg/day. After 4 days of treatment with either E2 or BPA, these mice developed chronic hyperinsulinemia, and their glucose and insulin tolerance tests were altered. These experiments unveil the link between environmental estrogens and insulin resistance. Therefore, either abnormal levels of endogenous estrogens or environmental estrogen exposure enhances the risk of developing type 2 diabetes mellitus, hypertension, and dyslipidemia.

The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance

http://old.ssmu.ru/ofice/f6/ginfuv/information/rodi/f4.pdf

Vaginal progesterone in women with an asymptomatic sonographic short cervix in the midtrimester decreases preterm delivery and neonatal morbidity: a systematic review and metaanalysis of individual patient data

Steroid hormones can act as chemical messengers in a wide range of species and target tissues to produce both slow genomic responses, and rapid non-genomic responses. Although it is clear that genomic responses to steroid hormones are mediated by the formation of a complex of the hormone and its cognate steroid-hormone nuclear receptor, new evidence indicates that rapid responses are mediated by a variety of receptor types associated with the plasma membrane or its caveolae components, potentially including a membrane-associated nuclear receptor. This review summarizes our current knowledge of membrane-associated steroid receptors, as well as details of structure–function relationships between steroid hormones and the ligand-binding domains of their nuclear and membrane-associated receptors. Furthermore, a new receptor conformational ensemble model is presented that suggests how the same receptor could produce both rapid and genomic responses. It is apparent that there is a cornucopia of new drug development opportunities in these areas.

Steroid-hormone rapid actions, membrane receptors and a conformational ensemble model.

Losel, Ralf M., Elisabeth Falkenstein, Martin Feuring, Armin Schultz, Hanns-Christian Tillmann, Karin Rossol-Haseroth, and Martin Wehling. Nongenomic Steroid Action: Controversies, Questions, and A...

Nongenomic Steroid Action: Controversies, Questions, and Answers

Steroid hormones may profoundly influence hemostasis; for example, as discussed for hormone replacement therapy, pregnancy and, being less obvious, for the ovarian cycle. We investigated primary hemostasis parameters using a platelet function analyzer (PFA-100) during the follicular and luteal phases in 18 healthy young women without oral contraceptives. During the follicular phase, the mean closure time (CT) was 164.7 +/- 56.7 s, and it decreased to 130.2 +/- 30.6 s in collagen/epinephrine cartridges in the luteal phase (P = 0.0095). No significant difference could be found for CT values in collagen/adenosine diphosphate cartridges during the follicular phase as compared with the luteal phase (97.2 +/- 24.2 s versus 89.6 +/- 18.4 s, P = 0.174). Negative correlations between the CT values in collagen/epinephrine cartridges and von Willebrand factor from both phases of the cycle were found (follicular phase: r = -0.53; luteal phase: r = -0.54). Fibrinogen and fibrinogen degradation products were significantly increased in the luteal phase (2.49 +/- 0.62 g/l versus 2.05 +/- 0.59 g/l and 0.12 +/- 014 versus 0.04 +/- 0.04, P = 0.02 for both parameters) as compared with the follicular phase. No significant differences could be detected for plasminogen, plasmin-antiplasmin complex, prothrombin fragment 1 + 2 and D-dimer between the groups. This study indicates that platelet function is periodically altered during the ovarian cycle due to the influence of progesterone and estrogen on von Willebrand factor concentrations.

Alterations in platelet function during the ovarian cycle.

In past decades, numerous epidemiological and clinical studies in women taking oral contraceptives revealed the impact of sex steroids on coagulation factors and the incidence of venous thrombosis. To date, only scarce data regarding the impact of oral contraceptives on platelet function are available. The aim of this study was to further elucidate the impact of sex steroids on platelet function. We conducted an observational study in young women using different types and dosages of monophasic oral contraceptives (OCs) compared to women not taking OCs. During the follicular phase, the mean closure time (CT) in Col/Epi was 168.0 +/- 64.9 s compared to 131.5 +/- 28.9 s during the luteal phase (p=0.012). In Col/Epi cartridges, no difference was detected between women taking second/third generation OCs and low-dose OCs (145.2 +/- 44.3 vs. 169.4 +/- 63.5, p=0.34). In contrast, mean Col/Epi values of women using anti-androgen-containing OCs were less (110.3 +/- 15.6 s) than in both other OC groups (p=0.03 for both comparisons). The same holds for Col/Epi values from women during the follicular- and luteal phases compared to women using anti-androgen-containing OCs (p=0.0002, p=0.013). Significant correlations between progesterone and platelet function in women not using OCs (p=0.02) could be found. In conclusion, the results of the study show that platelet function might be modulated by OCs and the female cycle. As for OCs, the main factor seems to be the progestagen. During the female cycle, the main impact on platelet function might be mediated by progesterone.

Effect of oral contraceptives and ovarian cycle on platelet function

A quick glance at rapid aldosterone action

Rapid effects of aldosterone on vascular cells: clinical implications

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