Meta-iodobenzylguanidine seen in the diagnosis of pathologic conditions of the adrenal medulla (pheochromocytoma)
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Biomedical subjects
Publications and source records attributed to D Scavo.
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An increase in morning fasting levels of plasma (P) renin activity (RA), aldosterone (A) and serum (S) angiotensin-converting enzyme (ACE) activity has been demonstrated in ascitic cirrhotic patients (ACP). Since both PRA and PA change biorhythmically in their time structure, the relationship of SACE activity with the components of the renin-angiotensin-aldosterone system (RAAS) was investigated in clinically healthy subjects (CHS) and ACP. Time-qualified data were chronobiologically analysed by means of the cosinor procedure to resolve and quantify the circadian rhythm (CR). The 24-hour mean levels of PRA, PA and SACE activity were found to be elevated in ACP as compared to CHS. The temporal variability of these analytes was found to be of periodic type along the 24-hour span in CHS, but not in ACP. The well-organized cyclicity in CHS is of relevant interest. PRA and PA cycles were found to phase in a clear antiparallelism with the SACE activity CR. The phase opposition may be, speculatively, related to the physiologic nature of ACE, whose activity is devoted to generate angiotensin II. The disappearance of SACE activity CR in ACP is in accordance with the abolition of PRA and PA cyclicity and suggests a role of liver in regulating the periodic time function of the RAAS and related components.
The Na,K-ATPase activity of erythrocyte membranes is markedly increased in normal-renin essential hypertensives. A temporal shift of the chronobiology of the erythrocyte-membrane-bound Na,K-ATPase in these patients is described. The disorder causes a loss of synchronism between the circadian rhythms of aldosterone and Na,K-ATPase. Such uncoupling phenomenon may explain the inversion of the day/night sodium excretion ratio and other disturbances of sodium metabolism found in essential hypertensives.
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Peripheral mononuclear (PMN) cells are known to produce ACTH-like immunoreactivity (ACTH-LIR) in vitro. Based on these findings the aim of this study was to find out whether thymopentin (the active pentapeptide of the native hormone thymopoietin) may stimulate ACTH-LIR production and release by cultured normal human lymphocytes. Thymopentin at concentration of 1 microgram/ml was capable of inducing ACTH-LIR release by normal human PMN cells (median 22 pg/ml) whereas ACTH-LIR inside cells was lower (median 11 pg/10(7) cells). The chromatographic characterization of the eluted material identified the presence of ACTH immunoreactive peptides with the elution characteristics of the precursors 31 K proopiomelanocortin, 22 K ACTH and 4.5 K ACTH, together with higher molecular weight material (greater than 43 K). These data demonstrate that thymopentin induces ACTH-LIR release by human lymphocytes, thus adding a novel factor to those already reported (corticotrophin releasing factor, lipopolysaccharide, viruses) capable of such function.
B-Endorphin (B-Ep), ACTH and cortisol circulating levels, before and after a two months therapy with a hypocaloric diet and an increase in physical exercise, were measured by RIA in 17 obese female subjects. After therapy, the body weight excess fell from 56.6 +/- 22.2% to 38.6 +/- 22.1% (p less than 0.01). Plasma levels of B-Ep decreased from 18.3 +/- 12.5 fmol/ml to 6.4 +/- 3.5 fmol/ml (p less than 0.01); those of ACTH from 46.8 +/- 22.8 pg/ml to 31.2 +/- 11.6 pg/ml (p less than 0.01); and those of cortisol from 15.9 +/- 4.6 micrograms% to 10.3 +/- 2.5 micrograms% (p less than 0.01). The reduction of the elevated plasma B-Ep levels found in obese subjects is related principally to the diet therapy. Thus, as shown in experimental animals, excessive feeding results in an increased hypothalamic-pituitary secretion of B-Ep.
Acute physical exercise stimulates the activity of the hypothalamus-pituitary-adrenal axis in man. In the present study we measured plasma adrenocorticotropin, beta-endorphin, beta-lipotropin and cortisol levels in 27 male trained athletes in basal conditions, 60 min before and immediately after an official competition. The endocrine responses were evaluated in different groups of athletes participating in races (100 m, 1500 m, 10,000 m) or in the disc throw. The athletes competing for the runs showed a statistically significant increase in plasma adrenocorticotropin, beta-endorphin, beta-lipotropin and cortisol levels after the race (P less than 0.01), whereas the disc throwers showed no significant change in the hypothalamus-pituitary-adrenal axis hormones after the competition. The percent increase in plasma adrenocorticotropin, beta-endorphin, beta-lipotropin and cortisol was higher in the athletes who run 1500 m and 10,000 m than in those participating in the short distance race (100 m). The present results showed that plasma proopiomelanocortin-related peptides and cortisol levels increase in trained athletes following running competition and that this increase is related to the duration of the physical exercise.
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Serum levels of aldosterone and cortisol were measured by radioimmunoassay in 15 patients with gestational diabetes, in 18 patients with Type 1 (insulin-dependent) diabetes, in 36 pregnant control women and in 10 non-pregnant control women. All subjects, on habitual sodium and potassium intake, were sampled in a supine position at 09.00 hours. Pregnant women were examined twice, during gestational week 32-34 and at delivery. Serum levels of aldosterone and cortisol were also measured in the umbilical cord blood of newborn babies of these diabetic and non-diabetic mothers. Serum levels of aldosterone in both gestational and Type 1 pregnant diabetic women were found to be consistently above the reference values of non-diabetic pregnant women. Abnormal serum levels of aldosterone were also observed in newborn infants of diabetic mothers. In contrast, serum levels of cortisol were not increased.
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In order to clarify the possible interaction between endogenous opioids and glucose homeostasis in obesity we studied Beta-Endorphin (B-Ep), ACTH, cortisol and insulin plasma levels in response to an oral glucose tolerance test (OGTT) in 8 females suffering from uncomplicated obesity and in 6 healthy volunteers of normal weight. Results were evaluated in terms of secretion areas subtracted from basal value. Basal glucose, insulin and B-Ep levels were significantly higher in the obese patients compared to controls, cortisol levels and ACTH were not statistically different between obese and normal subjects. During OGTT total areas of insulin secretion were significantly higher in the obese patients; cortisol, ACTH, B-Ep plasma levels did not change in controls, whereas obese patients showed a response to B-Ep which reached a peak at 60 minutes. The area of B-Ep response to OGTT in obese patients was significantly higher than in controls. On the basis of these results we may suggest that the opioid system belongs to the chain of neuroendocrine and metabolic events responsible for the origin and the growth of overweight. But the possibility exists that obesity itself can enhance the B-Ep secretion above all through overeating. In this regard it is to stress that glucose ingestion induces in obese patients, differently from normal subjects, insulin hypersecretion and the B-Ep secretion, possibly from gastro-enteric tract and/or pancreatic isles.
The circadian (about 24-hr) oscillating function of the renin-angiotensin-aldosterone system (RAAS) was investigated as a function of age in clinically healthy participants and in essential hypertensive patients. A peculiar age-related decline in the RAAS circadian mesor (rhythm-adjusted mean) and amplitude (variability from mesor) was found in the essential hypertensive patients. This finding suggests a nonphysiologic evolution in the tonic (24-hr mean level) as well as phasic (oscillating amplitude) circadian activity of the RAAS with increasing age. A relative hyperreninemic aldosteronism characterized the aged essential hypertensive patients.
The effects of a severe (10-20 mEq/24-h) but short-term (7-days) restriction in dietary sodium on 24-h blood pressure (BP) patterns were investigated in 20 normotensive volunteers (10 men, 10 women; 20-25 years old) by means of non-invasive automatic sphygmomanometric monitoring (recordings at 1-h interval) at home, with subjects in bedrest. Statistical methods used include bivariate Gaussian distribution analysis for systolic and diastolic BP bivariate discriminant analysis, periodic regression analysis with a 24-h period (cosinor method) and spectral analysis of time series. Casual BP measurements were unable to detect the tensinogenic effects, while the bivariate Gaussian analysis documented a total rearrangement in the pattern distribution to show discriminated values of BP after sodium restriction. A significant decrease (p less than 0.01) in the 24-h mean level (mesor) for systolic BP was observed. An increase in the extent of fluctuation (amplitude) for the circadian components was documented by the spectral analysis, mainly in diastolic BP patterns. Such a phenomenon of 'amplitude magnification' was not accompanied by a change in the repartition of the ultradian and circadian harmonic components. The extensive changes in the time structure support the hypothesis of an interaction of sodium regimen with the centrally-located oscillators which physiologically organize the circadian rhythmicity of BP.
The effect of a mild reduction in dietary sodium intake (-30 mEq/24 hr) and body weight (-2 kg/2 months) on circadian rhythms of urinary aldosterone (UA), sodium (UNa), potassium (UK), creatinine (UC) and volume (UV) have been investigated in nine clinically healthy subjects. The mild reduction in dietary sodium is associated with: (1) a decrease in the 24-hr excretion rate of UNa, UK and UV, and an increased mesor of UA and UC; (2) a lowered extent of the circadian variation for UNa, UK, UV and a greater amplitude for UA and UC (3) a later crest in the temporal phase for UK, UA, UC, an earlier phasic wave for UNa. The mild reduction in calorie intake resulting in a body weight loss is associated with a more pronounced decrease in the 24-hr excretion rate of UNa and UK, and in the extent of circadian fluctuation for UNa. Peculiar events are: (1) the decreased 24-hr excretion rate for UA, and the increased mesor for UV; (2) the extent variability increased for UV, decreased for UC. Such effect may have a practical resonance for heuristic physiology since the role of dietary sodium and food intake has been better clarified. Dietary sodium and food can be regarded as 'chronomodulatory agents' for the adrenal cortex since their adrenotropic influence is extended to the tonic as well as phasic secretion of aldosterone.
Normal-renin essential mesor hypertensives are characterized by a consistent increase in erythrocyte membrane-bound Na/K-ATPase activity. Low-renin essential hypertensives exhibit, in contrast, a lower activity in Na/K-ATPase of cell membranes. This study documents a third disorder characterized by a temporal shift in the rhythmic activity of the erythrocyte membrane-bound Na/K-ATPase in normal-renin hypertensives. The disorder causes the synchronism with the aldosterone circadian rhythm to be invariably lost. The uncoupling phenomenon could be invoked to explain the inversion in the day-night sodium excretion rate found in essential hypertensives. In addition, it suggests that the circadian rhythm in Na/K-ATPase is under the control of cycling factors other than aldosterone.