PubMed · 14374856
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B STREITMANN. 1954-11-01. [Erythroderma and adrenal cortex function].. https://pubmed.ncbi.nlm.nih.gov/14374856/
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OBJECTIVE: To determine the effects of a single course of maternally administered dexamethasone on preterm fetal sheep in utero. DESIGN: Prospective randomised controlled trial. SETTING: University laboratory. SAMPLE: Pregnant sheep at 0.7 of gestation. METHODS: Pregnant ewes at 103 days of pregnancy (term = 147 days) were given two intramuscular injections of vehicle (n= 7) or 12 mg of dexamethasone (DEX; n= 8) 24 hours apart. Fetuses were continuously monitored for five days. MAIN OUTCOME MEASURES: Fetal mean arterial blood pressure, carotid and femoral arterial blood flow and vascular resistance, heart rate, heart rate variability, fetal plasma cortisol and ACTH and fetal body movements. RESULTS: DEX injections led to an acute increase in mean arterial blood pressure with a rise in carotid and femoral vascular resistance, a fall in femoral arterial blood flow, and a brief fall in fetal heart rate followed by significant tachycardia. From 24 hours after the injections, mean arterial blood pressure and vascular resistance returned to control values, however, a mild tachycardia [200 (3) vs 184 (4) bpm, P < 0.05] and loss of the circadian pattern of fetal heart rate variability persisted until the end of recording. Plasma ACTH and cortisol were markedly suppressed by DEX (P < 0.05), with values returning to control levels 32 and 72 hours after the first injection, respectively. There was no effect on basal fetal heart rate variability, body movements, carotid arterial blood flow, or the circadian pattern of fetal heart rate. CONCLUSION: In contrast to previous experiments utilising direct fetal infusion of steroids, maternal administration of DEX was associated with only transient hypertension.
One mechanism for organ damage in individuals with arterial hypertension may be due to oxygen free radical production. This study was designed to localize free radicals in a microvascular network of mature spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. Because glucocorticoids play a role in pressure elevation of SHRs, we investigated their role in microvascular free radical formation. Oxygen radical production in mesentery was detected by tetranitroblue tetrazolium reduction to formazan aided by digital light-absorption measurements. Formazan deposits were observed in the endothelial cells and lumens of all microvessels and in lymphatic endothelia but were fewer in tissue parenchyma. The formazan distribution in younger (14-16 wk old) WKY rats and SHRs was heterogeneous with low values in capillaries and small arterioles/venules (<30 microm) but enhanced deposits in larger venules. Adrenalectomy served to reduce the formazan density in SHRs to the level of WKY rats, whereas dexamethasone supplementation of the adrenalectomized rats caused elevation in the larger venules of SHRs. In older (40 wk old) SHRs, formazan levels were elevated in all hierarchies of microvessels. After pressure reduction was employed with chronic hydralazine treatment, the formazan deposits were reduced in all locations of the microcirculation in both WKY rats and SHRs. Elevated formazan deposits were also found in lymphatic endothelium. These results suggest that oxygen free radical production is elevated in both high- and low-pressure regions of SHR microcirculation via a process that is controlled by glucocorticoids. Older SHRs have higher formazan levels than younger SHRs in all microvessels. Chronic hydralazine treatment, which serves to reduce arterial blood pressure, attenuates tetranitroblue tetrazolium reduction in WKY rats and SHRs even in venules of the microcirculation, which has no micropressure elevation. Free radical production may be a more global condition in SHRs and may not be limited to arteries and arterioles.
In the light of studies suggesting that transcription of the gene coding for manganese superoxide dismutase (MnSOD) is induced by ACTH in the rat adrenal gland, northern blot analysis was used to determine its mRNA distribution. It was found that mRNA coding for MnSOD is primarily present in the inner zones of the rat adrenal cortex, and not the glomerulosa. To investigate the functional relationships between MnSOD activity and expression and adrenocortical function, adrenals and blood were taken from animals pretreated with corticotrophin or betamethasone (Betnesol), or subjected to a low-sodium diet. MnSOD activity in inner zone mitochondrial fractions was enhanced by corticotrophin and by a low-sodium diet, but suppressed by betamethasone. Apparent cytosolic MnSOD activity, total cytosolic MnSOD and CuZnMn-SOD, and glomerulosa mitochondrial MnSOD all were unaffected. Steroid assays showed a clear correlation between circulating corticosterone and inner zone mitochondrial MnSOD, but none between aldosterone and glomerulosa MnSOD. Immunoblot analysis of MnSOD showed two apparent isoforms, at approximately 25 kDa and 75 kDa. There was a partial relationship between expression of the 75 kDa isoform and MnSOD activity, in that it was induced by corticotrophin. However, there was also a slight induction with betamethasone, and a low-sodium diet had no effect. The 25 kDa MnSOD isoform was unaffected by the treatments. The results suggest that MnSOD may have a specific role in the steroidogenic function of the fasciculata/reticularis of the rat adrenal, but not in that of the glomerulosa.