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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is generally believed that adrenal steroid hypertension is due to the 'mineralocorticoid' and/or 'glucocorticoid' activities of the steroid(s). The present study examines the blood pressure and metabolic effects of steroid hormone infusion in intact conscious sheep to assess the relative contributions of 'glucocorticoid' and 'mineralocorticoid' activity. Cortisol at 5 mg/h increased mean arterial pressure (MAP) but the effect was small (MAP + 10 mm Hg on day 5). This rate of infusion produces blood cortisol levels appropriate for maximal ACTH stimulation. Cortisol at 20 mg/hr produced hypertension (MAP + 25 mm Hg on day 5, p less than 0.01) but also produced the 'mineralocorticoid' effect of severe hypokalaemia. Dexamethasone at 1 mg/hr produced small increases in MAP but a profound fall in plasma [K]. Aldosterone at 80 microgram/hr (a pharmacological rate) produced hypokalaemia, urinary Na retention but no effect on MAP over 5 days. Thus, in short term infusion experiments, 'mineralocorticoid' effects are not associated with hypertension. Pharmacological concentrations of predominantly 'gluc-corticoid' steroid hormones produced hypertension but also exhibited substantial 'mineralocorticoid' activity. At levels approximating maximal physiological secretion, the rise in blood pressure was small. These results supported the contention that ACTH induced hypertension in sheep represents a mechanism different from a simple 'mineralocorticoid' or 'glucocorticoid' action.
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PMID:Comparison of the effects of 'glucocorticoid' and 'mineralocortocoid' infusions on blood pressure in sheep. 53 76

Eighty days after i.c. cryoextraction of the lens without any complications, intra- or postoperative, choroidal detachment was observed in a 68-year-old woman (hypertension, diabetes m..amaurosis of the right eye after central artery embolism). -Conventional decongestive drugs (Reparil, Tantum, Tanderil) had no effect. Within 6 days of treatment with microwaves, 2.5% Hydrocortisone and atropine eye-drops and Prednisolone (10 mg/die) internally there was complete regression of the detachment.
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PMID:[Late choroidal detachment after i.c. cryoextraction of the lens (author's transl)]. 95 74

Decrease in arterial pressure, mainly manifested in the first 5-10 days, was established in 111 patients with hypertension disease in functional and initial organic stage in the conditions of moderately high mountain (1870 m above sea level) after 25/20 days of complex climatic treatment including: active motor regimen, sun-air exposure and Pevzner diet No 10. Simultaneously the excretion of 17-hydroxicorticosteroids was increased in daily urine. Suprarenal cortex stimulation is best manifested after the first week and is kept till the end of the treatment. Cortisol plasma level was elevated in 42.7 per cent of the patients with hypertension disease with initial values under 15 mkg/100 ml plasma after three hours moderately severe physical activity, carried out in physiological thermal conditions and was decreased with 25.9 per cent with initial levels over 20 mkg/100 ml plasma. Parallely, 17-hydroxicoricosteroids secretion in urine was decreased as well as the systolic and diastolic arterial pressure.
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PMID:[Effect of climatic exposure and physical activity on plasma cortisol levels and urinary 17-hydroxycorticosteroid excretion in patients with hypertension]. 100 41

In a 31-year old woman with a six year history of headache and hypertension a diagnosis of primary aldosteronism was made on the basis of urine samples containing 45 mug/day of aldosterone. The preoperative systemic blood pressure was 240 mm Hg systolic and 120 mm Hg diastolic. The serum potassium level was 2.6 mEq/L and other laboratory findings were within normal limits. The patient was to undergo operation. Pre-medication consisted of oral pentobarbitone, intramuscular pethidine and atropine. For induction of anaesthesia, enflurane 2.0-2.5% maximum was given with O2 (21/min) and N2O (61/min); no intravenous agents were used. Suxamethonium chloride 40 mg was administered to facilitate endotracheal intubation. Anaesthesia was maintained with enflurane 1.5-2.0% with 50% N2O and O2. Tubocurarine 27 mg was given for muscle relaxation. When the tumour was manipulated, systemic arterial blood pressure was elevated again to 190 mm Hg systolic and 120 mm Hg diastolic. After removal of the tumour, the arterial pressure and heart rate were stable and recovery from anaesthesia was without circulatory or respiratory complications. Plasma aldosterone levels reached a maximum when the tumour was manipulated and fell to normal levels on the second post-operative day. Cortisol levels were not altered markedly even when the tumour was handled. These data imply that adrenocortical response to enflurane anaesthesia as jadged by plasma aldosterone levels would be different from that as estimated by plasma cortisol levels.
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PMID:Enflurane anaesthesia for removal of aldosterone producing adenoma. 126 18

Corticotrophin releasing hormone (CRH), dehydroepiandrosterone sulfate (DHEAS) and cortisol were measured in umbilical cord plasma obtained from 90 preterm and 98 term fetuses. Maternal plasma was obtained from 23 women who delivered preterm and from 23 women matched for gestational age who ultimately delivered term infants. Mean umbilical cord plasma CRH concentration was significantly higher in the preterm fetuses (n = 69, 538 +/- 63 pg/ml) compared to the term fetuses (n = 98, 280 +/- 22 pg/ml, P < 0.01). Mean DHEAS level in the preterm fetuses was 208 +/- 22 mg/dl (n = 56), cortisol level was 7 +/- 1 mg/dl (n = 58). Umbilical plasma CRH concentrations (808 +/- 170 pg/ml) were significantly higher at 24-27 weeks than at 28-31 or 31-34 weeks gestation. Cortisol levels (12 +/- 3 micrograms/dl) were highest at 24-27 weeks. Mode of delivery and the presence of labor did not affect fetal CRH levels. The highest fetal CRH levels were measured in the pregnancies complicated by hypertension as well as prematurity; however, fetal CRH levels remained higher in the preterm group compared to the term group when hypertensive pregnancies were excluded. Maternal plasma CRH levels were significantly higher in the group that delivered preterm compared to women who delivered at term matched for gestational age (1058 +/- 184 pg/ml compared to 456 +/- 71 pg/ml, P < 0.00).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotropin releasing hormone concentrations in umbilical cord blood of preterm fetuses. 130 8

ACTH and adrenocortical steroids have been known to raise blood pressure since their introduction into clinical practice. Our experimental studies in normal subjects show that ACTH reproducibly increases blood pressure in association with a rise in cardiac output, plasma and extracellular fluid volumes and exchangeable sodium. The rise in pressure is adrenally dependent and appears due to ACTH-induced increases in cortisol secretion. When ACTH is given by constant intravenous infusion, rates as low as 50 micrograms/day raise pressure. The increase in blood pressure is not dependent on, but modified by, dietary sodium content. Synthetic steroids (prednisolone, methylprednisolone, triamcinolone, dexamethasone) raise pressure in the absence of any increase in plasma volume or urinary sodium retention. Cortisol increases pressor responsiveness to endogenous and exogenous catecholamines, without evidence of any increase in sympathetic nervous activity. The role of this increased pressor responsiveness in ACTH/steroid-induced hypertension remains to be determined. There is some evidence from human studies that steroids may raise pressure by a hypertensinogenic mechanism, distinct from classical mineralocorticoid or glucocorticoid effects.
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PMID:Adrenocorticotrophin and steroid-induced hypertension in humans. 132 9

1. 11 beta-Hydroxysteroid dehydrogenase converts cortisol to inactive cortisone in man. In distal renal tubules, this inactivation protects mineralocorticoid receptors from cortisol. Congenital 11 beta-hydroxysteroid dehydrogenase deficiency and inhibition of 11 beta-hydroxysteroid dehydrogenase by liquorice or carbenoxolone result in cortisol-dependent hypokalaemia and hypertension. 2. 11 beta-Hydroxysteroid dehydrogenase is expressed in vascular smooth muscle. Both glucocorticoids and mineralocorticoids potentiate vascular responses to noradrenaline. 11 beta-Hydroxysteroid dehydrogenase activity may therefore influence vascular tone. 3. Experiments were performed in healthy subjects with and without 7 days of oral administration of 11 beta-hydroxysteroid dehydrogenase inhibitors (liquorice or carbenoxolone), and in a patient with congenital 11 beta-hydroxysteroid dehydrogenase deficiency. We measured the following parameters: dermal vasoconstriction after topical application of cortisol, forearm blood flow during brachial artery infusion of cortisol or noradrenaline, and blood pressure during systemic infusion of noradrenaline. 4. Cortisol-induced dermal vasoconstriction was increased by liquorice (23 +/- 6 to 52 +/- 7 units; P < 0.04) and in congenital 11 beta-hydroxysteroid dehydrogenase deficiency (87 units). In congenital 11 beta-hydroxysteroid dehydrogenase deficiency intraarterial infusion of cortisol caused vasoconstriction (20% reduction in blood flow in the infused arm) and accentuated the response to application of lower-body negative pressure, which stimulates sympathetically mediated vasoconstriction (35% reduction). However, intra-arterial infusion of cortisol had no effect in healthy subjects either with or without administration of liquorice. 5. Carbenoxolone potentiated both noradrenaline induced forearm vasoconstriction (P < 0.01) and pressor response (P < 0.001). 6. We conclude that 11 beta-hydroxysteroid dehydrogenase modulates the access of cortisol to vascular receptors and thereby influences vascular sensitivity to noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucocorticoids and blood pressure: a role for the cortisol/cortisone shuttle in the control of vascular tone in man. 132 32

11 beta-OHSD is an enzyme complex consisting of 11 beta-DH, converting cortisol to cortisone in man and an 11-keto-reductase performing the reverse reaction. Congenital deficiency of 11 beta-DH should be considered in any child presenting with mineralocorticoid hypertension and suppression of the renin-angiotensin-aldosterone axis. The keystone to diagnosis is the demonstration of a reduced daily production rate of cortisol and an increase in its plasma half-life. In the majority of cases diagnosis can be made from a urinary steroid metabolite profile indicating a high excretion of cortisol relative to cortisone metabolites. Cortisol is the responsible mineralocorticoid, and as such treatment with the pure glucocorticoid dexamethasone will prevent life-threatening hypokalemia, although additional anti-hypertensive drugs are usually required to control blood pressure. Liquorice and carbenoxolone, for years thought to be direct "agonists" of the mineralocorticoid receptor, in fact cause sodium retention through inhibition of 11 beta-DH. The demonstration of 11 beta-DH activity in the vasculature raises the possibility that it locally modules access of glucocorticoids to mineralocorticoid and possibly glucocorticoid receptors in the vessel wall. It remains possible that subtle alterations of this cortisol-cortisone shuttle are responsible for other forms of hypertension which are currently classified under the umbrella diagnosis of essential hypertension.
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PMID:The cortisol-cortisone shuttle and hypertension. 195 52

Hydrocortisone phonophoresis (HPP) on the affected joints or balneotherapy with iodine bromine baths as well as the complex of these two modalities were used to treat 197 patients with osteoarthrosis. Thirty-one of the patients had secondary arthrosis due to recurrent gout attacks. Monotherapy with HPP proved beneficial in affection of 1-2 joints whereas the baths appeared preferable in polyosteoarthrosis, its association with spinal osteoarthrosis, arterial hypertension. Combined application of HPP and the baths produced more pronounced and stable effect with the best relief recorded in polyosteoarthrosis, its progression, secondary synovitis.
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PMID:[The therapeutic use of iodide-bromide-sodium chloride baths combined with hydrocortisone phonophoresis in patients with osteoarthrosis and gout]. 207 38

Recent studies have shown the predictive power of abdominal distribution of adipose tissue for the development of cardiovascular disease, stroke, diabetes as well as strong associations to the previously known risk factors for these endpoints. The reason for the accumulation of abdominal fat might be due to an imbalance between cortisol and sex steroid hormones. Cortisol receptor density seems to be particularly high in abdominal adipose tissue, leading to expression of lipoprotein lipase activity primarily here. Progesterone and testosterone seems to counteract this, the former perhaps through competition with the cortisol receptor. Accumulation of intraabdominal fat, particularly in the tissues drained by the portal circulation, probably leads to high free fatty acid concentrations in the portal vein, because of the high lipolytic sensitivity of these tissues. This in turn seems to inhibit hepatic clearance of portal insulin, leading to peripheral hyperinsulinemia, insulin resistance, perhaps hypertension as well as hyperlipidemia via drive by free fatty acids of lipoprotein synthesis in the liver. These are risk factors for diabetes, cardiovascular disease and stroke. It is of interest that subjects with abdominal adipose tissue have several factors leading to increased cortisol and low sex steroid hormone secretion, including stress, high alcohol consumption and smoking. This might provide some of the background to this syndrome.
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PMID:Obesity and adipose tissue distribution as risk factors for the development of disease. A review. 214 Jan 8


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