The Journal of Steroid Biochemistry and Molecular Biology
Glucocorticoids but not mineralocorticoids modulate endothelin-1 and angiotensin II binding in SHR vascular smooth muscle cells
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Drug-induced endocrine blood pressure elevation
2020, Pharmacological ResearchCitation Excerpt :Studies addressing the role of the MR in cortisol-induced hypertension showed diminished mineralocorticoid effects upon co-administration of spironolactone, but no effect on blood pressure, suggesting that the mineralocorticoid effects are not solely responsible for cortisol-induced hypertension [139,140]. Increasing evidence even speaks against a major role of the MR in glucocorticoid-dependent hypertension but implicates other targets, such as altered nitric oxide synthase activity or increased expression of AT1 receptors (reviewed by [141–143]). These observations are further supported by the fact that dexamethasone, which has negligible MR activity [138], can also cause hypertension.
Developmental origins of cardiovascular disease: Impact of early life stress in humans and rodents
2017, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Numerous studies have demonstrated that acute or chronic exposure of the fetus to elevated maternal glucocorticoids during pregnancy programs the offspring for hypertension and cardiovascular disease (Moritz et al., 2003) (Ortiz et al., 2003, 2001). Additionally, glucocorticoids directly regulate blood pressure by increasing sodium and calcium intake within the vascular smooth muscle (Kornel et al., 1993) and by increasing vascular responsive to Ang II (Provencher et al., 1995) and noradrenaline (Bian et al., 1992). Nonetheless, few studies have addressed the long-term consequences of the exposure to elevated corticosterone levels during postnatal life using animal models.
Hydrogen sulfide is involved in dexamethasone-induced hypertension in rat
2015, Nitric Oxide - Biology and ChemistryCitation Excerpt :Moreover, an increase in endogenous levels of vasoconstrictor agents i.e. norepinephrine and angiotensin II, as well as in calcium influx, has been reported as plausible mechanisms of steroid-induced hypertension [6–9]. The presence of glucocorticoid receptor (GR) in vascular smooth muscle and endothelial cells implies a direct role for GCs in vasculature tone control [10–13]. Genetic and molecular studies have demonstrated that suppression of GR in vascular smooth muscle attenuates, but does not prevent, the development of dexamethasone (DEX)-induced hypertension [14].
Cardiovascular effects of Boophone disticha aqueous ethanolic extract on early maternally separated BALB/C mice
2013, Journal of EthnopharmacologyCitation Excerpt :The present results suggest that Boophone disticha may have possible associated anxiolytic-like activity which may alter pathophysiological changes in behavior and endocrine system associated with repeated early MS previously described as increased plasma corticosterone release and elevated NGF levels in the hippocampus which can affect the development and maturation of specific organs related to blood pressure control and maintenance, such as heart, vasculature, kidney and brain (Igosheva et al., 2004; Daniels et al., 2009). Glucocorticoids can directly regulate blood pressure, increasing sodium and calcium uptake by vascular smooth muscle (Kornel, 1993) and increasing vascular responsiveness to angiotensin II (Provencher et al., 1998) and noradrenaline (Bian et al., 1992; Walker and Williams, 1992). These glucocorticoid-induced changes in both central and effector sites of the cardiovascular control may be reflected in enhanced cardiovascular responses to acute stress seen here in MS mice and seem to be decreased by treatment with Boophone disticha freeze dried aqueous ethanolic crude extract.
Primary epiphyseal arteriopathy in a mouse model of steroid-induced osteonecrosis
2013, American Journal of PathologyCitation Excerpt :ON of the femur and humerus was prevented in a rabbit model when a nitrate skin patch was administered at the same time as intramuscular administration of methylprednisolone at 20 mg/kg of body weight.32 Glucocorticoid receptors have been shown in the media of the canine aorta,33 and numerous in vitro studies have provided evidence that the glucocorticoid receptor is present in both the vascular smooth muscle34–36 and the vascular endothelium.35,37,38 In addition to the expected effect of changes in gene expression, studies have indicated that they may mediate the effect of glucocorticoids on the influx of Na+ or Ca2+ into cells.35,39
Dexamethasone stimulates endothelin-1 gene expression in renal collecting duct cells
2012, SteroidsCitation Excerpt :While collecting duct cells express 11βHSD-2 and are not typically activated by endogenous glucocorticoids, ET-1 and dexamethasone have documented interactions in other cells types. For example, glucocorticoids decrease ET-1 binding to vascular smooth muscle cells from wild-type and spontaneously hypertensive rats [40,41]. Dexamethasone-induced Edn1 mRNA may also be clinically relevant in sodium transporting epithelia.