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Biomedical subjects

D C Kem

Publications and source records attributed to D C Kem.

At least 55 records · Page 3Linked to original sources
PubMed1978

Plasma aldosterone response to ACTH in primary aldosteronism and in patients with low renin hypertension.

ACTH alpha 1-24 was infused at incremental rates of 12.5-200 mIU/30 min in dexamethasone-suppressed hypertensive patients on a regular sodium diet. The plasma aldosterone response to this stimulus in 8 patients with hyperaldosteronism due to an adrenal aldenoma and 11 with adrenal hyperplasia was significantly greater at all infusion rates (P less than 0.05) when compared with the response in 6 normal subjects on a similar diet. This responsiveness to ACTH in the patients with primary hyperaldosteronism was similar to that of the normal subjects on a low sodium diet. Twelve patients with low renin and 6 patients with normal renin essential hypertension were similarly studied. There was no significant difference in the median aldosterone response between these 2 groups and the normal subjects on a normal diet, but the response was significantly lower compared with that in patients with primary hyperaldosteronism. These data show that patients with hyperaldosteronism from an adrenal adenoma or hyperplasia have a consistent and exaggerated response to ACTH. The hyper-responsiveness is not apparently shared by the majority of patients with low renin essential hypertension and does not support the concept that this group is an intermediate form of primary aldosteronism. Individual patients within this group, however, may have such a response and might be identified by this type of testing.

Adenoma↗
PubMed1977

Interaction of 16beta-hydroxydehydroepiandrosterone with renal mineralocorticoid receptors.

A previously unidentified mineralocorticoid, 16beta-hydroxydehydroepiandrosterone (16beta OH-DHEA) has recently been isolated from urine extracts of patients with low-renin hypertension and reported to possess one-fortieth the mineralocorticoid potency of aldosterone by bioassay. However, using a radioreceptor assay, we demonstrate the affinity of 16beta-OH-DHEA for renal 3H-aldosterone receptors to be only 0.011 per cent that of unlabeled aldosterone. 16beta-OH-DHEA therefore would not be expected to possess significant mineralocorticoid properties unless its mechanism of action involves binding to a unique class of renal receptors. Until these discrepancies between bioassayable mineralocorticoid activity and affinity for mineralocorticoid receptors can be resolved, the role of 16beta-OH-DHEA in the pathogenesis of low-renin hypertension remains speculative.

Aldosterone↗
PubMed1976

Circadian rhythms of serum renin activity and serum corticosterone, prolactin, and aldosterone concentrations in the male rat on normal and low-sodium diets.

To investigate the control of aldosterone secretion, non-stress levels of serum aldosterone, corticosterone, and prolactin, and renin activity were determined at 4-h intervals during 24-h light-dark cycles in adult male rats on regular and low-sodium diets. Circadian rhythms of plasma aldosterone, prolactin, and corticosterone concentrations and of serum renin activity were demonstrated during a regular sodium diet. When the rats were on a low-sodium diet, a circadian rhythm of serum corticosterone and aldosterone concentration was observed, but there was no circadian variation in serum renin activity or in serum prolactin concentration. Serum aldosterone concentration correlated with serum corticosterone concentration (r = 0.48) and serum renin activity (r = 0.36) during a low-sodium diet. Serum prolactin concentration did not correlate with serum aldosterone concentration or serum osmolality. These data are compatible with a role for renin and ACTH, but not for prolactin, in the modulation of aldosterone secretion in the rat.

Aldosterone↗
PubMed1976

The intravenous furosemide test: a simple way to evaluate renin responsiveness.

To identify patients with low-renin hypertension, we measured plasma renin activity after the administration of 40 mg of furosemide intravenously and 30 minutes of upright posture in 127 normotensive subjects and 363 patients with essential hypertension. Plasma renin activity 30 minutes after intravenous furosemide was found to be closely correlated to the level found after either 2 or 4 h of standing or 3 days of a low-salt diet plus 2 h of upright posture. Renin responsiveness was significantly lower in hypertensive patients, blacks, and women, compared with normotensive subjects, whites, and men respectively. The level of plasma renin activity in most normal white subjects was greater than 1.0 ng/ml - h and in most normal blacks was greater than 0.5 ng/ml - h. It was below those levels in 23% of white hypertensive and 25.2% of black hypertensive patients respectively. The mean level of plasma renin activity fell with increasing age of hypertensive patients. This procedure is recommended as a safe, easy, and reliable test for assessing renin responsiveness and identifying the low-renin state.

Adult↗
PubMed1976

The role of ACTH in the episodic release of aldosterone in patients with idiopathic adrenal hyperplasia, hypertension, and hyperaldosteronism.

The relationship of plasma aldosterone concentration to its identified stimuli was examined in three patients with hypertension, hyperaldosteronism, and idiopathic adrenal hyperplasia. Four patients with hyperaldosteronism due to adrenal adenomas served as controls. Plasma aldosterone, cortisol, sodium, and potassium concentrations and renin activity were measured in blood samples taken at 20 minute intervals from 2 A.M. to 8 A.M. during recumbency and sleep. The tests were performed on all patients following a regular sodium diet both before and after short-term treatment with dexamethasone. Two of the three subjects with adrenal hyperplasia were re-examined after 2 weeks of dexamethasone therapy. All four control patients with adenomas had episodic increases of plasma aldosterone which were significantly correlated with those of plasma cortisol (r = +0.48 to +0.90). This confirms the previously reported relationship between aldosterone and ACTH in such patients. Two patients with idiopathic adrenal hyperplasia had a similar secretion pattern and a highly significant correlation of the two hormones (r = +0.76 and +0.77); one did not (r = 0.13). Short-term dexamethasone pretreatment attenuated the episodic release pattern and partially suppressed the mean plasma concentrations of aldosterone in the four patients with an adenoma and in the two patients with idiopathic hyperplasia whose plasma aldosterone and cortisol concentrations were positively correlated. There was no such effect in the third patient. The first two patients with idiopathic hyperplasia were subsequently retested following 2 weeks of dexamethasone treatment to determine if the episodic secretion pattern of plasma aldosterone would correlated with other stimuli following this period of ACTH suppression. One showed little change from the pattern observed after short-term glucocorticoid treatment. The second had a similarly blunted aldosterone response until ACTH secretion led to a resumption of episodic changes in plasma aldosteerone concentrations. These data indicate that ACTH frequently is the dominant stimulus of the episodic secretion of aldosterone in patients with either adrenal adenomas or hyperplasia. When ACTH is suppressed, the hypersecretion of aldosterone is presumably sustained by an intrinsic adrenal abnormality or by an as yet unidentified stimulus.

Adenoma↗
PubMed1975

A direct radioimmunoassay of corticosterone in rat serum.

A direct radioimmunoassay of corticosterone is described requiring as little as 1-2 mul of rat serum. After methanol inactivation of CBG, serum was assayed with a relatively specific antibody raised against corticosterone-21-hemisuccinate. While this antibody has a significant cross-reaction with cortisol, prior purification is not necessary since cortisol is not produced in the rat.

Animals↗
PubMed1975

The effect of dexamethasone on the control of plasma aldosterone concentration in normal recumbent man.

In order to evaluate the control of the circadian rhythm of plasma aldosterone concentration in man, plasma aldosterone, cortisol, sodium and potassium concentrations, and plasma renin activity (PRA) were measured in samples obtained at 20-minute intervals from 0200 to 0800 in sodium repleted (180 mEq. per day of diet) and sodium depleted (22 mEq. per day of diet) normal subjects. During sodium replete studies, plasma aldosterone and cortisol concentrations were significantly correlated (p greater than 0.01) in all 4 subjects. Plasma aldosterone also correlated with PRA (p greather than 0.01) in 2 subjects and with potassium (p greater than 0.01) in one. Episodic increases in plasma aldosterone concentration were observed despite suppression of ACTH by dexamethasone treatment. Plasma aldosterone concentrations were significantly correlated with PRA (p greater than 0.05 and p greater than 0.01) in only 2 of 4 subjects under these conditions. Following sodium restriction, plasma aldosterone concentrations were not significantly correlated with plasma cortisol and only infrequently with either PRA or potassium. When dexamethasone was administered during the low sodium diet, correlations with PRA (p greater than 0.001) were seen in 2 of 3 subjects and with potassium (p greater than 0.01) in 1 of 3 subjects. There was no significant correlation between plasma aldosterone and sodium concentration during any of the studies. These results are compatible with the concept that the relative importance of PRA, ACTH, and potassium in inducing changes in aldosterone production during the early morning hours is partially dependent upon dietary sodium, but also varies between individuals studied during similar sodium diets. The episodic alterations of plasma aldosterone concentration continued after ACTH was suppressed by dexamethasone pretreatment. These changes, in the absence of a consistent significant correlation with PRA and sodium and potassium concentrations, further suggest that another factor(s) may be important in controlling aldosterone production in recumbent normal subjects.

Administration, Oral↗
PubMed1973

Circadian rhythm of plasma aldosterone concentration in patients with primary aldosteronism.

Plasma aldosterone, cortisol, and renin activity were measured in nine recumbent patients with hyperaldosteronism, including seven with adenomas, one with idiopathic hyperplasia, and one with glucocorticoid suppressible hyperplasia. All had peak values of plasma aldosterone concentration from 3 a.m. to noon and lowest values at 6 p.m. or midnight. This rhythm was similar to the circadian pattern of plasma cortisol in the same patients. When these data were normalized to eliminate the wide variation in ranges of plasma aldosterone and cortisol between individuals, there was an excellent correlation (r = + 0.87, P < 0.005) between the two hormones. In contrast, plasma aldosterone concentrations did not correlate with plasma renin activity before or after normalization of data. Short term suppression of ACTH by administration of dexamethasone eliminated the circadian variation of plasma aldosterone in both patients with hyperplasia and in four of five patients with adenomas, while it markedly altered the rhythm in the fifth. Similar doses of dexamethasone were administered to four normal subjects and did not flatten the circadian rhythm of plasma aldosterone. These data suggest that patients with primary aldosteronism have a circadian rhythm of plasma aldosterone mediated by changes in ACTH.

Adenoma↗
PubMedDate not supplied

Epinephrine fraction of adrenal vein blood in pheochromocytoma.

Variability in the levels of epinephrine (E) and norepinephrine (NE) in adrenal vein blood is thought to preclude their usefulness in caval sampling studies for localizing abdominal pheochromocytoma. In this study we demonstrate, in three patients, that the fraction of the total catecholamine level in the adrenal effluent represented by E (E fraction) may differentiate the normal adrenal medulla from the gland containing a pheochromocytoma. This observation is additionally supported by calculations of the E fractions, from adrenal venous E and NE reported recently, in three other patients with pheochromocytoma. Our data, combined with those from the literature, yield a mean E fraction, in adrenal vein blood, of 63.8 +/- 11.4 (SD)% for seven normal adrenal medullae, and of 28.5 +/- 4.8% for five glands bearing pheochromocytoma. The use of this parameter for lateralizing adrenal pheochromocytoma is suggested if other procedures are unable to demonstrate the tumor.

Adrenal Gland Neoplasms↗