An association between hyperinsulinemia and hypertension has been suggested by epidemiological surveys. To assess whether this association is independent of the presence of other hyperinsulinemic states, such as obesity and glucose intolerance, we measured the insulin response to oral glucose in a group of middle-aged moderately obese [144 +/- 4% overweight (mean +/- SEM)] patients (n = 18) with essential hypertension (174 +/- 5/104 +/- 2 mm Hg) and normal glucose tolerance. Normotensive subjects (n = 17) with normal glucose tolerance, matched for age and degree of overweight, served as the control group. The mean insulin response to glucose was twice as high in the hypertensive patients (25.8 +/- 0.2 mU/ml X 2 h) as in the normotensive subjects (11.3 +/- 0.2; P less than 0.001), yet the glucose incremental area was 3-fold higher in the former (10.9 +/- 1.0 g/dl X 2 h) than in the latter (3.5 +/- 0.7; P less than 0.001), thus indicating more severe insulin resistance. In the hypertensive group, systolic blood pressure levels were directly correlated with the 2-h plasma insulin values (r = 0.75; P less than 0.001). Furthermore, the 2-h plasma insulin value and the degree of overweight accounted for 65% of the variation in the systolic blood pressure in a multiple regression model (r = 0.81; P less than 0.001). We conclude that in obesity, the occurrence of hypertension marks the presence of additional hyperinsulinemia and insulin resistance, independent of any impairment of glucose tolerance.

Age, ingestion of a strong acid, leucocytosis, deep gastric ulcers, and gastric necrosis are predictive of death after caustic ingestion. A risk score system including these predictors may be useful in prognostic evaluation.

Inthis study we have examined the effect of the administration of oxytocin on basal blood concentrations of insulin, glucagon, cortisol, growth hormone, and on the dynamic secretory response of these hormones to intravenous glucose administration (0.33 g/kg) in basal condition and after the injection of 3 IU (1 plus 2 IU/1 h) or 6 IU (2 plus 4 IU/ 1 h) of oxytocin (6 subjects for each group). The highest dose of oxytocin (6 IU) used significantly increased insulin secretion in response to intravenously administered glucose. No significant change of insulin secretion was observed with 3 IU of oxytocin. Glucagon, cortisol, and growth hormone response to intravenous injection of glucose was not affected by oxytocin (3 or 6 IU) administration. These results suggest that high doses of oxytocin affect β-cell function in normal man.

Nicotine from cigarette smoking has been found to increase circulating concentrations of cortisol in man (Wilkins, Carlson, Van Vunakis, Hill, Gritz and Jarvik 1982). After evaluation of literature data, a direct effect on the adrenal gland cannot be excluded (Rubin and Warner 1975); however, this effect more likely depends on an increase of ACTH secretion by the pituitary (Conte-Devolx, Oliver, Giraud, Gillioz, Castanas, Lissitzky, Boudouresque and Millet 1981), secondary to a modification of some hypothalamic neurotransmitter (Wilkins et al. 1982). Among others, the noradrenergic System seems to have an important role in the regulation of ACTH secretion (Weiner and Ganong 1978). Recently it has been reported that hypothalamic noradrenergic nerve terminal System is regulated by cholinergic nicotinelike receptors (Andersson, Fuxe, Eneroth and Agnati 1982), and their Stimulation by Clonidine, a selective noradrenergic receptor agonist (Struyker, Boudier and Van Rossum 1972), is capable of reducing ACTH and cortisol secretion in man (Lanes, Herren, Palacios and Moncada 1983). Therefore, it is possible that the effect of cigarette smoking is mediated by a modification of this pathway. The present investigation was undertaken in order to verify whether pretreatment with Clonidine modifies ACTH-cortisol secretion in response to cigarette smoking. Materials and Methods7 normal healthy men (27-34 years) consented to participate in the smoking studies. All were habitual cigarette smokers. All studies were performed at 09.00 a.m. after an overnight fast and withholding from smoking. Subjects were in the supine position throughout the period of the tests. A 19-gauge scalp vein needle was inserted into an arm vein and kept patent by slow saline (NaCl 0.9%) infusion and used for blood sampling. Blood samples were obtained at -20, -10 and 0 before smoking. Clonidine HCl (0.15 mg) diluted in physiological saline (NaCl 0.9%) was injected i.v. (over a 10 min period) at -10. On a different day saline was injected instead of Clonidine for a control test. Tests were carried Fig. 1 Effect of smoking nicotine (• • ) under basal conditions and after Clonidine (0.15 mg) injection (• •) on plasma ACTH and cortisol levels. Each point represents the mean of 7 observations ± SE. Differences obtained under control and experimental conditions were statistically significant from 20 min to 50 min for ACTH and from 20 min to 60 min for cortisol.

This study was performed in order to investigate the dopaminergic mechanism involved in the control of arginine-vasopressin (AVP) secretion in normal men. Plasma AVP concentrations were measured before and after the administration of an i.v. bolus of 10 mg metoclopramide or domperidone to twelve healthy males. Metoclopramide, a cerebral and peripheral antagonist of dopaminergic receptors, significantly stimulated AVP secretion, whereas domperidone, a dopamine antagonist which does not cross the blood-brain barrier, was without effect. These data suggest that metoclopramide stimulates the release of AVP by blocking dopaminergic receptors in structures located inside the blood-brain barrier. Alternatively, it is possible that the stimulation of AVP release induced by metoclopramide does not occur through inhibition of dopamine receptors but rather through interaction with other neuroendocrine pathways.

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Patients with familial adenomatous polyposis are at risk of significant neoplasia. The natural history of precancerous lesions might be related to surgical treatment of colorectal neoplasms.

Abstract. iv administration of oxytocin decreases plasma ACTH-cortisol levels in normal men. In contrast, naloxone, a specific opioid antagonist, stimulates cortisol release, suggesting that opioid peptides exert an inhibitory control on ACTH-cortisol secretion. The present study was carried out in an attempt to determine whether an opioid pathway mediates oxytocin action; therefore, we evaluated the effect of naloxone on the decrease of cortisol induced by oxytocin. Six normal men were treated iv with oxytocin (2 IU as a bolus), naloxone (4 mg as a bolus plus 10 mg infused for 2 h) or a combination of the 2 drugs. Plasma cortisol levels were determined in samples taken before and 2 h after drug treatment. As expected, administration of oxytocin significantly decreased cortisol secretion, while naloxone had a stimulatory effect on plasma cortisol levels. When oxytocin injection was followed by administration of naloxone, cortisol levels remained unchanged; thus, naloxone abolished a cortisol decrement in response to oxytocin. These findings show that in man oxytocin requires an active opioid system in order to produce its inhibitory action on ACTH-cortisol secretion, suggesting that this effect of oxytocin could be mediated by an opioid pathway.