Relationship between natriuresis and changes in plasma atrial natriuretic factor, renin activity and aldosterone levels in fasting obese subjects.

This study was conducted to assess whether changes in atrial natriuretic factor (ANF) secretion could account for the natriuresis of the early phase of fasting. To this end, 8 AM (supine) and 10 AM (standing) plasma ANF concentrations were determined daily and compared with plasma renin activity and aldosterone levels in 8 obese subjects submitted to a 7-day total fast. Depiste constant daily sodium intake (51 mmol), urinary sodium excretion increased from 35 +/- 7 to 109 +/- 8 mmol/day after 4 days of fast (p less than 0.001) and declined thereafter. Urinary ketone excretion progressively increased over the whole period of fasting (p less than 0.001). Interestingly, fasting induced a decrease in plasma ANF concentrations (p less than 0.05). A contrast analysis revealed no significant change in ANF during the initial natriuretic phase of fasting but a decrease at the end of fasting averaging 36% (p less than 0.05) and 18% (p less than 0.05) at 8 and 10 AM respectively. In contrast, plasma aldosterone rose during fasting (p less than 0.05), the difference being significant at the end of fasting (p less than 0.01). Plasma renin activity and cortisol did not change significantly over the fasting period. Postural and/or diurnal changes of ANF, aldosterone, renin and cortisol were preserved during fasting (p less than 0.01). Postural changes of ANF were, however, attenuated at the end of fasting (p less than 0.05). These data indicate that the fasting natriuresis cannot be explained by changes in ANF levels but that the loss of sodium may contribute to a decline of basal ANF levels, with an attenuation of their physiological postural changes, and to a stimulation of the aldosterone secretion

Detection and identification of endothelin-1 immunoreactivity in rat and porcine thyroid follicular cells.

Endothelin-1 immunoreactivity (irET-1) was observed in rat and porcine thyroid glands. Using a radioimmunoassay for endothelin-1, the mean concentration in extracts of rat and porcine thyroid glands were 0.75 pg/mg +/- 0.03 (n = 4) and 1.5 pg/mg +/- 0.2 (n = 8) (mean +/- SE) respectively. Gel-filtration and reverse-phase HPLC showed that ir ET-1 eluted in a position identical to synthetic endothelin-1. In addition, immunohistochemical study showed that irET-1 is located within epithelial follicular cells. No immunostaining was seen in parafollicular C-cells nor in parathyroid

The Effects of Glucose-ingestion and Fasting On Plasma-immunoreactive Beta-endorphin, Adrenocorticotropic Hormone and Cortisol in Obese Subjects

It has been demonstrated that opioid peptides are involved in the stimulation of food intake in rats and that the circulating beta-endorphin levels are increased in genetically obese rodents. Therefore, to assess whether the changes in food intake may influence circulating beta-endorphin levels in obese subjects, plasma beta-endorphin, ACTH and cortisol concentrations were determined in obese patients after an oral glucose load and during a 7-day total starvation. Baseline plasma beta-endorphin concentrations were significantly higher in obese patients than in control normal-weight subjects, while ACTH and cortisol levels were similar in both groups. Plasma beta-endorphin, ACTH and cortisol concentrations were not affected by the ingestion of 75 g glucose, neither were plasma beta-endorphin concentrations modified during prolonged starvation. Moreover, the lack of nycthemeral variations in beta-endorphin levels, documented before and during starvation while plasma ACTH and cortisol were significantly reduced in the evening, suggests that some extra anterior pituitary sources or some obesity-related changes in beta-endorphin metabolism may contribute to the pool of circulating beta-endorphin in obese subjects. On the other hand, even the extreme changes in nutritional conditions, such as total food deprivation or glucose ingestion, are devoid of any detectable influence on circulating beta-endorphin levels

Atrial natriuretic factor during percutaneous transluminal coronary angioplasty.

To study the release of plasma atrial natriuretic factor (ANF) and to explain the mechanism underlying its increase during myocardial ischemia, we measured plasma ANF and mean pulmonary capillary wedge pressure (PCW) before, during and after percutaneous transluminal coronary angioplasty (PTCA) in eight patients. All patients were free of calcium channel antagonists and beta-blocking drugs. Evidence of myocardial ischemia was observed in all patients with an increase of PCW from 3.2 +/- 1.2 to 10.6 +/- 2.9 mm Hg (mean +/- SD; p less than 0.001). Heart rate and mean blood pressure did not change significantly. We observed an increase of plasma ANF during PTCA, from 53 +/- 24 to 100 +/- 37 pmol/L (mean +/- SD; p less than 0.005). There was a correlation between absolute values of ANF and PCW before and during PTCA (r = 0.64, p less than 0.01). After PTCA, ANF levels remained increased for at least twenty minutes (p less than 0.005 vs basal state) despite a decrease in PCW. Thus, increase of PCW during this very short-term left ventricular ischemic dysfunction induces an increase of plasma ANF, which persists during a certain time when PCW returns to normal