Biomedical subjects
Publications and source records attributed to C R Edwards.
In five patients with inappropriate lactation and amenorrhoea or impotence brom-ergocryptine was found to suppress the lactation and to diminish the raised plasma prolactin levels. The responses to treatment suggest that there may be an inverse relationship between prolactin secretion and gonadotrophin secretion in man.
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Using a bioassay dependent on the development of a lactogenic response in rabbit mammary tissue cultured in vitro, prolactin distinct from immunoreactive growth hormone has been found in the plasma of patients of both sexes with inappropriate lactation with and without evidence of pituitary tumours. It has also been found in one patient with primary hypothyroidism and galactorrhoea, and in another during chlorpromazine therapy, but not in nine patients with gynaecomastia without galactorrhoea. Plasma prolactin levels were examined in seven patients during oral glucose tolerance tests: no change occurred in the four patients with pituitary tumours, but the levels were suppressed in the three patients with normal pituitary fossae. Prolactin appears to be a distinct pituitary hormone in man, as in animals, and also to be aetiologically related to states of inappropriate lactation.
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A 22-year-old woman with primary hypothyroidism developed amenorrhoea and galactorrhoea during oral contraceptive therapy. Investigation showed high levels of circulating prolactin which rose in response to insulin-induced hypoglycaemia and were suppressed by an oral glucose load. After treatment with thyroxine normal periods returned, the galactorrhoea improved, and the prolactin levels fell to undetectable levels. The results of the prolactin and human growth hormone assays confirm that it is possible to distinguish between human growth hormone and human prolactin.
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It has been demonstrated that somatostatin (SRIF) can suppress hypophyseal and extrahypophyseal hormones; moreover, many studies have shown that SRIF inhibits frusemide-induced hyperreninemia in normal man, and renin and aldosterone in renovascular hypertension, possibly through a beta-adrenergic block. To further investigate the possible aldosterone-inhibiting effect of somatostatin, we have carried out in vitro studies using isolated perfused rat zona glomerulosa cells suspended in Bio-gel. Paired columns were set up and the cells stimulated using either angiotensin II, ACTH, serotonin or potassium. One column was perfused with somatostatin (3-4 ng/ml) and the other was used as a control. Aldosterone was measured by highly specific direct radioimmunoassay. Somatostatin significantly blocked the aldosterone response to angiotensin II but not to ACTH, serotonin or potassium. The inhibitory effect of somatostatin persisted as long as it was added to the medium; the aldosterone response to angiotensin II was progressively restored after discontinuation of the SRIF infusion. From these data it might be suggested that the inhibitory effect of somatostatin on aldosterone production is not cAMP-dependent, since ACTH maintains its stimulatory capacity. The recent demonstration of the presence of specific somatostatin receptors on the rat adrenal cells suggests that its inhibitory effect could be mediated by the second messenger system rather that the interaction with angiotensin II receptors.
A previously described direct radioimmunoassay for plasma aldosterone has been modified to enable direct measurement of the steroid in saliva. The specificity of the method has been demonstrated by assay after high pressure liquid chromatographic purification of saliva extracts. Assay of matched plasma and saliva samples taken from normal subjects during unrestricted and controlled sodium intakes, either under basal conditions or while undergoing ACTH stimulation or dexamethasone suppression, confirms that salivary aldosterone values provide a good reflection of levels in plasma. Mean salivary aldosterone values are approximately one-third of those in plasma. Sampling immediately upon waking appears to provide reliable values for salivary aldosterone, and the potential application of this technique to the screening of hypertensive patients is discussed.
Hypertension is strongly predicted by a low birthweight:placental weight ratio. Two independent models have been described to explain this association; less than optimal maternal protein nutrition leading to fetal undernutrition, or glucocorticoid excess. Pregnant rats were fed diets containing 18 per cent casein (control) or 9 per cent casein, balanced for energy. On day 20 of gestation the pregnancies were terminated and placentae collected for determination of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) activity. Placental 11 beta HSD normally protects the fetus from the effects of maternal glucocorticoids. Activity was specifically attenuated by mild protein restriction (33 per cent in activity), whilst activities of glucocorticoid-insensitive control enzymes were unchanged and glucocorticoid-inducible glutamine synthetase activity was increased (27 per cent), relative to activity in placentae from control animals. The nutritional manipulation during pregnancy significantly increased systolic blood pressure (17 mmHg) in the resulting offspring in early adulthood. A possible common pathway whereby maternal environmental factors may influence fetal and placental growth and programme disease is inferred.
We evaluated the possibility that there is enhanced conversion of cortisol (F) to cortisone (E) in obese children. IC-E was measured from 15 lean children aged 12.7 +/- 2.2 years, body mass index Z-score (BMI-SD) = -0.35 +/- 0.82, IC-F = 197 +/- 70 nM/l and 9 obese children aged 12.3 +/- 3.2 years, BMI-SD = + 4.7 +/- 2.1, IC-F = 149 +/- 53 nM/l. IC-E was higher in lean children 76 +/- 25 nM/l compared to obese 60 +/- 11 nM/l (p < 0.04). There was no difference in the ratio of IC-E/IC-F between lean 0.40 +/- 0.10 and obese subjects 0.42 +/- 0.09 (p < 0.06). IC-E was directly correlated with IC-F: IC-E = 0.25 x IC-F + 26 (n = 24, r2 = 0.57, p < 0.0001). In a multiple regression model (overall r2 = 0.32, p < 0.02), IC-E was related to BMI-SD inversely (p < 0.0054) and influenced as well by interaction of BMI-SD with sex (p < 0.043), IC-E being lower in boys with increasing body mass. In childhood, obesity is associated with decreased plasma IC-E and IC-F levels, the ratio of IC-E/IC-F is independent of body mass. Reduced IC-E levels in obese children are most likely due to the impact of body mass on IC-F.
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