hCG: its pancreatic and duodenal receptors and in vivo electrolyte secretion in female rats

A state of fluid flux probably resulting from ion movement across the plasma membrane occurs during early pregnancy or trophoblastic disease, manifesting as emesis or hyperemesis gravidarum or hydatidiform moles. In emesis or hyperemesis gravidarum, excessive secretion induced by a humoral agent may trigger vomiting by distending and activating the gastrointestinal (GI) tract mechanoreceptors. This agent may be human chorionic gonadotropin (hCG). High-affinity hCG binding sites similar to those in the ovary were found in the duodenum and pancreas of female rats, with dissociation constant values of 0.11 ± 0.02, 1.9 ± 0.6, and 4.7 ± 3.5 nM, respectively. The isoelectric point for duodenal and ovarian proteins was 5.5. With the use of two antisera directed against amino acid residues 24–33 and 239–249 of the lutropin receptor, positive immunohistochemical staining was seen in smooth muscle, Brunner’s glands, parasympathetic ganglia, crypt cells, and blood vessels of the duodenum, in zymogen granules of acini, and in intralobular ducts and blood vessels of the pancreas. Under nonreducing conditions, 150- and 170-kDa proteins were seen, through Western blot analysis, in the pancreas, duodenum, and ovary. Administration of hCG to female rats in vivo caused a significant increase in[Formula: see text] and K+ secretion from the duodenum and pancreas. We hypothesize that during pregnancy hCG stimulates excessive secretion of electrolytes (and fluid) into the upper GI tract, which culminates in the vomiting during pregnancy.

Are the Changes of Mood in Children with Coeliac Disease Due to Abnormal Serotonin Metabolism?

Children with untreated coeliac disease are characteristically unhappy and after a few days of treatment with a gluten-free diet their mood improves. This improvement in mood can be rapidly reversed by introducing gluten into their diet again which suggests that a humoral agent could be involved in this process. As serotonin is a neurotransmitter in the brain and abnormalities of serotonin metabolism have been reported in coeliac disease, this biogenic amine could be the humoral agent that mediates the changes of mood in coeliac disease. In this review the relationship between the mood changes in coeliac disease and serotonin metabolism will be further examined.

The Causative Agent in Atrial Receptor Diuresis in the dog is a Low Molecular Weight, Lipophilic and Weakly Acidic Substance

1. Stimulation of atrial receptors by distension of a balloon in the left atrium of anaesthetized dogs results in a reflex diuresis mediated by a humoral agent of unknown identity. 2. In previous investigations, a substance was recovered in a low molecular weight fraction from Bio-Gel P-2 (100-1800 daltons) and shown to be related to the reflex diuresis. 3. In this investigation, the active Bio-Gel P-2 fraction was partitioned with ethyl acetate at pH 11.0, with subsequent partition of the aqueous phase with ethyl acetate at pH 7.4; the activity of the humoral agent was soluble in ethyl acetate at pH 7.4. 4. These investigations suggest that the humoral agent is a low molecular weight, lipophilic and weakly acidic substance. 5. The substance is not antidiuretic hormone (ADH) as vasopressin is insoluble in ethyl acetate at pH 7.4.

Hypercalcaemia of Malignancy: Evidence for a Non-Parathyroid Humoral Agent with An Effect on Renal Tubular Handling of Calcium

1. The renal handling of calcium was examined in 31 patients with hypercalcaemia of malignancy. Results were compared with those from patients with primary hyperparathyroidism, and normal controls rendered hypercalcaemic by calcium infusion. 2. On relating the urinary calcium excretion indices to serum calcium values, inappropriately low rates of urinary calcium excretion were generally found in patients with malignancy associated hypercalcaemia. Further, the pattern of urinary calcium excretion in these subjects was similar to that found in patients with primary hyperparathyroidism. 3. These observations suggest that, in many solid tumours, the development of hypercalcaemia may be attributable to a humoral mediator with a parathyroid hormone-like effect on renal tubular calcium reabsorption. 4. The relatively frequent occurrence of hypercalcaemia in malignant disease thus may be partially explained by the presence of this humoral agent, which may impair the renal excretion of an increase in filtered calcium load, whether due to bone metastases, or humorally mediated osteolysis.

Metabolic control in a state of decreased activation: modulation of red cell metabolism

Very little is known in depth of the biochemical and physiological changes induced at the cellular level by human behavioral states. For study of the physiology of behavior at this level, the erythrocyte may be useful, because it is readily available and its metabolism and metabolic control are comparatively well understood. In this report we describe a marked decline of red cell glycolytic rate induced by the transcendental meditation technique (TM). This decline was significantly correlated with decreased plasma lactate concentration and with relaxation as indicated by electrodermal response. The occurrence of sleep was not correlated with the metabolic changes. The observed lack of variation of blood pH, blood gases, glucose, and hematocrit in this behavior implies that the decrease of erythrocyte metabolism is not an epiphenomenon of respiratory change or substrate availability. Based upon further measurements indicating persisting alteration of the red blood cell, we suggest the possibility of attachment of a humoral agent(s) to the cell in the mechanism of this effect. This behavioral effect is unique, and the effector(s) responsible may increase our understanding of metabolic control of the erythrocyte and of TM.

A Circulating Humoral Pressor Agent in Dahl S Rats with Salt Hypertension

1. In Dahl S rats becoming hypertensive while on a diet of high NaCl content there appears to be a blood-borne humoral agent which produces vasoconstriction in a bioassay using the isolated hindquarters of rats. 2. This vasoconstrictor effect strongly suggests the presence of a humoral pressor agent or the lack of a vasodilator agent in the blood of hypertensive S rats. 3. The vasoconstrictor effect is not due to high renin concentrations. 4. This humoral vasoconstrictor action could partly account for the high vascular resistance in the hypertensive S rat.