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

Pheochromocytoma (PHEO) occasionally associates with pathological lesions of the adrenal cortex. In most of them, ectopic adrenocorticotropic hormone (ACTH) produced by PHEO resulted in bilateral adrenocortical hyperplasia. The coexistence of PHEO and pre-clinical Cushing's syndrome (PCS) of the same adrenal gland has rarely been reported. We report on a patient and discuss the peculiar diagnostic aspects of this entity. A 52-yr-old Turkish woman was hospitalized at Farabi Hospital for further examinations of a right adrenal mass that was incidentally discovered by abdominal ultrasonography during examinations for abdominal bloating and "gas" in other hospital. The patient had a history of palpitations, nervousness, sweating and heat intolerance. On admission, her blood pressure was 140/90 mmHg. A physical examination revealed no signs of an excessive production of adrenocortical steroids such as in CS. Tension Holter monitoring revealed paroximal hypertension attacks (183/105 mmHg). Urinary catecholamines were markedly increased. Her serum cortisol concentrations ranged from 5 to 17 microg/dl, whereas ACTH levels were undetectable. Cortisol was not suppressed on the overnight 1 mg oral dexamethasone suppression test (DST), 2-day low-dose dexamethasone suppression test (DST). Abdominal computed tomography and magnetic resonance imaging studies revealed a solid round tumor approximately 4 cm in diameter, located in the right adrenal gland. A 131 lodine-metaiodobenzylguanidine (131 I-MIBG) scan revealed uptake within tumor in the right adrenal gland. Right adrenalectomy was performed; the surgical specimen revealed PHEO and adrenocortical hyperplasia. To our knowledge, the present report is a rare case of PHEO combined with PCS in the same adrenal gland.
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PMID:Pheochromocytoma combined with pre-clinical Cushing's syndrome in the same adrenal gland. 1611

We examined the effect or dietary doses of caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) on adrenocortical responses to behavioral stress in borderline hypertensive (BH) men using a randomized, double-blind, caffeine-placebo crossover design. Cortisol levels were assessed in BH men and matched normotensive (NT) controls at rest and in response to 35 min of continuous work on a psychomotor task alternating with mental arithmetic. Caffeine at rest elevated cortisol among BHs hut not among NTs. Both groups showed significant cortisol responses to caffeine combined with the tasks. These findings may have implications for the dietary use of caffeine in persons at risk for hypertension when faced with stressful situations.
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PMID:Adrenocortical effects of caffeine at rest and during mental stress in borderline hypertensive men. 1625 Jul 78

An increasing number of people live near airports with considerable noise and air pollution. The Hypertension and Exposure to Noise near Airports (HYENA) project aims to assess the impact of airport-related noise exposure on blood pressure (BP) and cardiovascular disease using a cross-sectional study design. We selected 6,000 persons (45-70 years of age) who had lived at least 5 years near one of six major European airports. We used modeled aircraft noise contours, aiming to maximize exposure contrast. Automated BP instruments are used to reduce observer error. We designed a standardized questionnaire to collect data on annoyance, noise disturbance, and major confounders. Cortisol in saliva was collected in a subsample of the study population (n = 500) stratified by noise exposure level. To investigate short-term noise effects on BP and possible effects on nighttime BP dipping, we measured 24-hr BP and assessed continuous night noise in another subsample (n = 200). To ensure comparability between countries, we used common noise models to assess individual noise exposure, with a resolution of 1 dB(A). Modifiers of individual exposure, such as the orientation of living and bedroom toward roads, window-opening habits, and sound insulation, were assessed by the questionnaire. For four airports, we estimated exposure to air pollution to explore modifying effects of air pollution on cardiovascular disease. The project assesses exposure to traffic-related air pollutants, primarily using data from another project funded by the European Union (APMoSPHERE, Air Pollution Modelling for Support to Policy on Health and Environmental Risks in Europe).
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PMID:Hypertension and Exposure to Noise near Airports (HYENA): study design and noise exposure assessment. 1626 98

Aldosterone is the principal endogenous mineralocorticoid in humans and regulates salt and water homeostasis. Cortisol, the major glucocorticoid, has high affinity for the mineralocorticoid receptor; however, 11beta-hydroxysteroid dehydrogenase type 2 converts cortisol to the inactive steroid cortisone in aldosterone target cells of the kidney, thus limiting the mineralocorticoid action of cortisol. Deoxycorticosterone (DOC) binds to the mineralocorticocoid receptor with high affinity and circulates at concentrations comparable to aldosterone. Severe DOC excess as is seen in 17alpha- and 11beta-hydroxylase deficiencies causes hypertension, and moderate DOC overproduction in late pregnancy is associated with hypertension. Here, we demonstrate that DOC is inactivated by the 20-ketosteroid reductase activity of the human AKR1C3 isozyme. Immunohistochemical analyses demonstrate that AKR1C3 is expressed in the mineralocorticoid-responsive epithelial cells of the renal cortical and medullary collecting ducts, as well as the colon. Our findings suggest that AKR1C3 protects the mineralocorticoid receptor from activation by DOC in mineralocorticoid target cells of the kidney and colon, analogous to cortisol inactivation by 11beta-hydroxysteroid dehydrogenase type 2.
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PMID:Deoxycorticosterone inactivation by AKR1C3 in human mineralocorticoid target tissues. 1633 83

The hormones with a strong influence on the lipid spectrum and the development of atherosclerosis include cortisol, growth hormone and oestrogens. Cortisol accelerates atherosclerosis both through dyslipidemia and through an increase in visceral fat, hypertension, increased insulin resistance and the development of reduced glucose tolerance which may result in diabetes mellitus. Even when a cortisol excess disappears, as is the case of patients cured of Cushing syndrome, arterial walls remain permanently vulnerable to the atherosclerotic process. In conditions involving a lack of growth hormone, dyslipidemia develops and increases the burden on the cardiovascular system if not treated in a timely manner by the substitution of growth hormone. Oestrogens have a double effect: they have an anti-atherogenic effect on artery walls that are not yet damaged by an atherosclerotic process, but where atherosclerosis has already developed they have a prothrombotic effect and destabilise the atheromatous plaques. If oestrogen is to be used as protection against the onset of atherogenesis, it is necessary to start in a period when the atherosclerotic process has not yet begun to damage the woman's arterial walls and it is best to use natural hormones (estradiol) and to prevent endometriosis it should be combined with crystalline progesterone applied locally--inravaginally. Oestrogens should be given in small doses, preferably parenterally. Even this will not prevent genetic oestrogen effects though.
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PMID:[How corticoids, growth hormone and oestrogens influence lipids and atherosclerosis]. 1757 71

Cushing's syndrome (CS) during pregnancy is a rare nosology with only a few cases reported in the literature. Misdiagnosis is common, as the syndrome may be easily confused with preeclampsia or gestational diabetes. CS during pregnancy is usually associated with severe maternal and fetal complications. A high degree of clinical awareness is therefore required to avoid miscarriage or premature delivery. We report an 18-year old female referred to our institution with amenorrhea and truncal obesity. Physical examination revealed cushingoid characteristics, including mild hypertension (130/100 mmHg). She was also found to be 8 weeks pregnant. A provisional diagnosis of CS was made based on plasma cortisol and adrenocorticotropin hormone (ACTH) measurements but the patient did not receive any relevant therapy. She eventually gave birth to a healthy full-term infant via vaginal delivery. A right adrenal adenoma was diagnosed post-labor and was subsequently treated with surgical resection. The patient's condition remained stable and 19 months after the adrenalectomy she gave birth to a second healthy full-term infant. Hydrocortisone (30 mg/day) was administered throughout the second gestation. Six months post-labor the treatment was discontinued after a normal hypothalamic-pituitary-adrenal (HPA) axis was ascertained.
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PMID:Cushing's syndrome in pregnancy: report of a case and review of the literature. 1772 9

1. Decreased nitric oxide (NO) availability is thought to be a feature of cortisol-induced hypertension in humans. 2. We hypothesized that, accordingly, the threshold for a depressor response to NO should be decreased by cortisol treatment. 3. We re-analysed data from a study of baroreflex function in normal men treated with cortisol using glyceryl trinitrate (GTN). 4. Cortisol treatment increased blood pressure and decreased the threshold dose of GTN for a fall in systolic and mean blood pressure. 5. These data support the notion that glucorticoid hypertension is associated with reduced NO bioavailability.
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PMID:Decreased threshold for the nitric oxide donor glyceryl trinitrate in cortisol-induced hypertension in humans. 1797 74

Obesity, lipid disorders, type 2 diabetes, high blood pressure and coronary heart disease are frequently encountered in wealthy populations. All these disorders frequently occur as clusters, constituting the metabolic syndrome. It is currently admitted that insulin resistance plays a central role in the pathogenesis of this syndrome. Stress responses include activation of the sympathetic nervous system and stimulation of epinephrine and cortisol release. These hormones may over the long term reduce insulin sensitivity. Cortisol may also favour the development of central obesity. In healthy individuals, mental stress increases heart rate, but simultaneously decreases vascular resistance in skeletal muscle. This results in a moderate increase in blood pressure, and an acute increase in insulin-mediated glucose disposal. In obese patients, mental stress elicits responses which differ widely from those of healthy individuals. While mental stress enhances catecholamine-mediated energy expenditure in obese patients to the same extent as in lean subjects, it fails to decrease systemic vascular resistance due to endothelial dysfunction. This leads to enhanced blood pressure responses and the absence of stimulation of glucose disposal in obese subjects during mental stress. It can be hypothesized that repeated professional or social stress may activate the sympathoadrenal system, resulting in high cortisol levels, stimulation of the sympathetic nervous system, and epinephrine secretion. All these factors may eventually lead to the development of central obesity and insulin resistance. Furthermore, the blood pressure responses to mental stress may be enhanced in insulin-resistant individuals, favouring the development of vascular complications.
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PMID:Stress and metabolism. 1837 Jul 4

Fat is stored around the abdomen in both subcutaneous and intra abdominal (visceral) sites. Visceral fat is associated in its own right with a set of metabolic abnormalities, including non insulin dependent diabetes, hypertension and dyslipidaemias. States of marked hypercortisolaemia, for example Cushing's syndrome, lead to the preferential accumulation of visceral fat. Since melancholic depression is known to be associated with elevated plasma Cortisol levels, this review explores whether depressed patients are prone to excess visceral fat storage, with the subsequent risk of developing the associated metabolic disturbances. Though the literature is limited, there is evidence that intra abdominal fat is increased in major depression. There is also evidence that depression is associated with increased risk of death from cardiovascular disease. Is visceral fat and its association with metabolic abnormalities the link between depression and physical illness?
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PMID:Melancholic depression and abdominal fat distribution: a mini-review. 1901 89

Severe arterial hypertension is a hallmark of Cushing syndrome which occurs in 80% of the patients. Additionally, persistent cortisol excess induces obesity, hyperinsulinemia with disturbed glucose tolerance and dyslipidemia which all contribute to the development of hypertension and its deleterious sequelae. Cortisol effects are mediated through diversely distributed intracellular glucocorticoid and mineralocorticoid receptors which are protected by the 11-beta-hydroxysteroiddehydrogenase type 2 in cells of some organs (i.e. kidney) but not in other. A highly complex clinical picture evolves in case of hypercortisolism due to the ubiquitous distribution of steroid receptors with different affinity and binding capacities for glucocorticoids. The present review focuses on the cortisol induced changes in blood pressure regulation which contribute to the development of hypertension.
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PMID:[Glucocorticoids and hypertension]. 1909 17


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