Glucocorticoids regulate both phorbol ester and calcium ionophore-induced endothelial prostacyclin synthesis

Rosenstock, Moti; Katz, Shikma; Danon, Abraham

doi:10.1016/s0952-3278(97)90517-2

Cited by 13 publications

(3 citation statements)

References 34 publications

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“…For all three groups, each experiment lasted 3 h. of many investigations. Some studies report that glucocorticoids cause hypertension by inhibition of cyclo-oxygenase (Rosenstock et al 1997) and nitric oxide (NO) synthase (NOS) (Mangos et al 2000), increased synthesis of endothelin-1 (Koshino et al 1998), up-regulation of dihydropyridine sensitive L-type calcium channels (Takimoto et al 1997) and other pathways associated with increases in intracellular calcium concentrations (Steiner et al 1989, Hayashi et al 1991, Kato et al 1992, Brem et al 1999, Clifton et al 2002.…”

Section: Anesthesia and Surgical Preparationmentioning

confidence: 99%

Effects of acute treatment with dexamethasone on hemodynamic and histopathological changes in rats

Ekerbiçer

İnan

Tarakç

et al. 2012

Biotechnic & Histochemistry

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We assessed the time-dependent effects of intraperitoneal (i.p.) and intravenous (i.v.) application of dexamethasone (Dexa) on the mean arterial blood pressure (MAP), heart rate (HR) and total blood volume (TBV). We evaluated also the relation between the effects and immunoreactivities of transforming growth factor-beta (TGF-β), epithelial nitric oxide synthase (eNOS), interleukin-1 beta (IL1-β) and vascular endothelial growth factor (VEGF) in rat brain, lung and kidney tissues. Rats were anesthetized and while still breathing spontaneously, a tracheotomy and femoral vein and artery catheterizations were performed. To determine TBV using the hemodilution method, 2 ml albumin-electrolyte solutions were applied by i.v. injection. Group 1 (control group) received a 1 ml bolus injection of physiologic saline, Group 2 received 15 mg/kg and Group 3 received 75 mg/kg Dexa i.p. The hematocrit was measured at 10, 20, 60 and 120 min. For each animal, the values of MAP, HR and TBV were measured within 2 h. For immunohistochemical evaluation, anti-TGF-β, anti-eNOS, anti-IL1-β and anti-VEGF primary antibodies were tested using the avidin-biotin-peroxidase method. TBV was decreased in Group 1 and the increase in MAP was statistically significant. HR values increased slightly. None of the values changed significantly in Group 2. Although TBV was unchanged in Group 3, the decrease in MAP was statistically significant. HR values increased, but the increase was not statistically significant. Mild IL1-β immunoreactivity and moderate TGF-β, eNOS and VEGF immunoreactivities were observed in the brain, lung and kidney samples in Group 1. Increased eNOS immunoreactivity in the kidney samples were observed in Group 2. eNOS immunoreactivity was as strong in the brain and the kidney samples in Group 3. Decreased VEGF immunoreactivity was observed in the lung and kidney tissues in Group 3. Significantly decreased TGF-β immunoreactivity was observed in all tissue samples in Group 3. The decreased MAP values in Group 3 differed from those in Groups 1 and 2. Despite increased eNOS immunoreactivity, especially in brain and kidney, the decrease in VEGF immunoreactivity in Group 3, especially lung and kidney, were consistent with a drop in blood pressure.

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Section: Anesthesia and Surgical Preparationmentioning

confidence: 99%

Effects of acute treatment with dexamethasone on hemodynamic and histopathological changes in rats

Ekerbiçer

İnan

Tarakç

et al. 2012

Biotechnic & Histochemistry

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“…The response to glucocorticoid release may comprise a suppressive mechanism to limit earlier stress activated responses (39,32). In the vascular endothelium, glucocorticoid has proven to suppress the production of vasodilators such as prostacyclin and NO (24,37,48); it has also been linked to the synthesis of the vasoconstrictor thromboxane (16).…”

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confidence: 99%

Inhibitory effect of glucocorticoid on coronary artery endothelial function

Rogers

Bonar

Estrella

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Acute and chronic stresses are implicated in cardiovascular diseases including coronary artery disease. The present study was designed to examine the direct effects of the stress hormone cortisol on nitric oxide (NO) release and endothelial NO synthase (eNOS) expression in cultured bovine coronary artery endothelial cells (BCAEC). Nitrate, nitrite, and NO (NO(x)) were measured by the chemiluminescence method. At 24 h after treatment, cortisol (1 nM-10 microM) produced a dose-dependent decrease in NO(x) release, which was attenuated in the presence of the 11beta-hydroxysteroid dehydrogenase inhibitor carbenoxolone (3 microM). In accordance, eNOS protein levels were significantly decreased by cortisol in a dose-dependent manner. Cortisol pretreatment significantly increased the rate of eNOS protein degradation in the presence of cycloheximide. In addition, cortisol pretreatment decreased ATP-induced intracellular Ca(2+) elevation and NO(x) release in BCAEC. The presence of glucocorticoid receptors in BCAEC was demonstrated by Western blot. The results suggest that cortisol, through activation of glucocorticoid receptors, suppresses NO(x) release in BCAEC by downregulating eNOS proteins and inhibiting intracellular Ca(2+) mobilization. Decreased NO(x) is likely to result in an increase in contraction of coronary arteries, leading to a decrease in coronary blood flow.

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“…Interestingly, glucocorticoids stimulate an increase in peak [Ca 2? ] i response to vasoconstrictors in VSMC in vitro and in vivo [34], and suppress the production of vasodilators such as prostacyclin and nitric oxide (NO) in vascular endothelium [39,40]. In coronary endothelial cells, cortisol is able to suppress, through activation of glucocorticoid receptors, the NO release by down-regulating endothelial NO synthase proteins and inhibiting Ca 2?…”

Section: Discussionmentioning

confidence: 99%

Coronary microvascular function in patients with Cushing’s syndrome

et al. 2012

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The aim of the study was to evaluate patients with Cushing's syndrome the coronary flow reserve (CFR), an index of coronary microvascular function. Fifteen newly diagnosed patients with Cushing's syndrome (1 male/14 females; mean age 45 ± 11 years), were selected for having no clinical evidence of ischemic heart disease. Twelve patients had pituitary-dependent Cushing's disease and three had an adrenal adenoma. Fifteen subjects matched for age, sex, and major cardiovascular risk factors were used as controls. Coronary flow velocity in the left anterior descending coronary artery was investigated by transthoracic Doppler echocardiography at rest and during adenosine infusion. CFR was obtained as the ratio hyperemic/resting diastolic flow velocity. A reduced coronary reserve (hyperemic/resting ratio ≤ 2.5) was found in 5/15 Cushing patients and 4/15 controls. In all patients with abnormal CFR, epicardial coronary stenosis was excluded by multi-slice computed tomographic coronary angiography. CFR was inversely related to urinary cortisol in patients with endogenous hypercortisolism (Spearman's rho = -0.57, P = 0.03), while no correlation was found in controls. Coronary microvascular function, as assessed by CFR, is pathologically reduced in a considerable number of patients with Cushing's syndrome without clinical symptoms of ischemic heart disease and in the absence of epicardial coronary artery lesions, as well as in controls matched for cardiovascular risk factors. The presence of comorbidities can explain this early coronary abnormality in both patients and controls. Whether urinary cortisol may be a predictor of coronary microvascular function in the setting of patients with Cushing's syndrome, needs further investigation.

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Glucocorticoids regulate both phorbol ester and calcium ionophore-induced endothelial prostacyclin synthesis

Cited by 13 publications

References 34 publications

Effects of acute treatment with dexamethasone on hemodynamic and histopathological changes in rats

Effects of acute treatment with dexamethasone on hemodynamic and histopathological changes in rats

Inhibitory effect of glucocorticoid on coronary artery endothelial function

Coronary microvascular function in patients with Cushing’s syndrome

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