Increased Sensitivity and Accuracy of Phaeochromocytoma Diagnosis Achieved by Use of Plasma-Adrenaline Estimations and a Pentolinium-Suppression Test

Brown, Morris J.; Allison, D J; Jenner, David; Lewis, Peter J.; Dollery, C T

doi:10.1016/s0140-6736(81)90058-1

Cited by 113 publications

(23 citation statements)

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“…Administration of cortisol, 1 1 -deoxycortisol, corticosterone, DOC and aldosterone together fail to reproduce the haemodynamic consequences of ACTH (Fan et al, 1975); addition to this cocktail of 17-hydroxyprogesterone and 17,2O-dihydroxyprogesterone mimics exactly the consequences of ACTH administration (Coghlan et al, 1976). It has been proposed that, in this model, these two additional steroids are acting at a distinct 'hypertensinogenic' receptor and that ACTH hypertension in the sheep is dependent on steroid binding to this receptor (Butkus et al, 1982;Whitworth et al, 1983a). In man, however, the situation is less complex and it seems likely that the effects of cortisol alone are qualitatively similar to those produced by ACTH and that ACTH hypertension is a consequence of cortisol excess (Connell et al, 1987b).…”

Section: Glucocorticoid Hypertensionmentioning

confidence: 99%

“…Stimulation tests have the attendant risks of provoking phaeochromocytoma crisis and should no longer be used (Sheps & Maher, 1968). An early suppression test was described using pentolinium (Brown et al, 1981), which acts as a sympathetic ganglion blocker, but this has now been superseded by the centrally acting alpha2 agonist, clonidine. In normal subjects, clonidine inhibits central sympathetic nervous system outflow and so reduces plasma noradrenaline levels.…”

Section: Glucocorticoid Hypertensionmentioning

confidence: 99%

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Hormones and Hypertension

Fraser

Davies

Connell

1989

Clinical Endocrinology

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The importance of changes in hormone secretion in human hypertension is a complex problem and too large to be dealt with in uniform detail in a short review. The subject encompasses not only the effects on blood pressure of primary endocrine disorders but also hormonal changes secondary to increased blood pressure. Some aspects are more fully understood than others and have been the subjects of relatively recent detailed reviews. Where this is the case, the current review has summarized the present position and cited reviews and key papers, in order to reserve space for more controversial and less well understood conditions such as the hypertension of growth hormone, thyroid hormone or glucocorticoid excess. CORTICOSTEROIDSThe human adrenal cortex synthesizes and secretes a large number of steroid hormones, biosynthetically interrelated with each other and with qualitatively and quantitatively different biological activities. The two major categories of compound are the adrenal androgens (androstenedione, dehydroepiandrosterone and testosterone) which, as far as is known, are not important in blood pressure control and will not be considered further (although there exist experimental models of hypertension which may be androgendependent), and the corticosteroids. These C21 steroids of the pregnane series exert two main types of action, mineralocorticoid and glucocorticoid effects, and excess secretion of either has widespread repercussions, particularly for neuromuscular function and the control of salt and water metabolism. Mineralocorticoids act mainly on the distal nephron via specific receptor activation to promote sodium reabsorption (with associated changes in extracellular fluid and plasma volume) and increased potassium and proton excretion, so that excess activity is characterized by hypokalaemia and a metabolic alkalosis. Aldosterone is the major mineralocorticoid in man but deoxycorticosterone (DOC) and corticosterone also have significant activity. More recently discovered compounds-18-hydroxy DOC, 18-oxocortisol and several compounds modified at position 19 (19-hydroxy or 19-nor)-may also contribute to the total mineralocorticoid action of the adrenocortical secretion (see review by Fraser & Padfield, 1985). Cortisol is the major human glucocorticoid. Glucocorticoids promote liver glycogen and protein synthesis but are catabolic in most other tissues, increasing lipolysis and protein R. Fraser et al.breakdown and reducing glucose uptake from the circulation. However, the kidney also possesses specific glucocorticoid receptors and, under experimental conditions, glucocorticoids can be shown to promote both natriuresis and kaliuresis, at least partly by raising glomerular filtration rate (GFR) and also to modulate Na+-H+ exchange in the proximal nephron (Davis & Howell, 1953;Mahnensmith & Aronson, 1985; Kinsella et al., 1985). Excess of either mineralocorticoid or glucocorticoid activity is associated with hypertension.The control of adrenocortical function is similarly complex and the subject of sev...

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Section: Glucocorticoid Hypertensionmentioning

confidence: 99%

Section: Glucocorticoid Hypertensionmentioning

confidence: 99%

Hormones and Hypertension

Fraser

Davies

Connell

1989

Clinical Endocrinology

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“…In healthy subjects, the relative contribution of the heart to the total norepinephrine spillover is 2-3% 21 and that of adrenals only 2%. 22 However, the relative contribution of the cardiac sympathetic nerves to norepinephrine plasma levels could substantially change under various pathological conditions, such as essential hypertension, heart failure and IHD. 19,23 In addition, plasma norepinephrine levels are determined at least in part by the rate of neurotransmitter "clearance" (i.e.…”

Section: Discussionmentioning

confidence: 99%

Plasma Catecholamines and Ischemic Heart Disease

Slavikova

Kuncová

Topolčan

2007

Clinical Cardiology

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SummaryPlasma levels of norepinephrine and epinephrine were measured in 84 patients aged 56 ± 9 (mean ± SD) years with chronic ischemic heart disease (IHD), anterior acute myocardial infarction (AMI), posterior AMI, acute or chronic IHD associated with various types of electrical instability and in the control subjects. During the first day of hospitalization, plasma epinephrine levels were higher in patients with AMI in both localizations and chronic IHD in comparison with control values. There were no significant differences in plasma epinephrine levels among these groups of patients. However, in the same time period, plasma norepinephrine concentrations in patients with chronic IHD and posterior AMI did not differ from the control values; in patients with anterior AMI they reached by ∼ 60% higher values than in the control group. Moreover, all myocardial lesions showing different types of electrical instability were associated with increased plasma levels of both norepinephrine and epinephrine. In conclusion, high plasma levels of epinephrine may result from sympathoadrenal activation. High plasma levels of norepinephrine in patients with anterior AMI and no change in patients with posterior AMI suggest a rather myocardial than an extramyocardial origin of plasma norepinephrine level in anterior AMI. Norepinephrine released from the ischemic area might contribute to the electrical instability of the myocardium and generation of dysrrhythmias.

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“…Pentolinium suppresses sympathetic overactivity in patients with primary hypertension, and a normal result effectively excludes a phaeochromocytoma. 2 An abnormal result is an indication for diagnostic localization with MRI, CT or a metaiodobenzylguanidine (MIBG) scan. MIBG scanning is not sensitive enough to exclude phaeochromocytoma (sensitivity 77-90%) but is useful in instances where CT or MRI have failed to localize a biochemically proven tumour.…”

Section: Commentmentioning

confidence: 99%