Separation of rabbit ileum mucus secretion from electrolyte and water secretion by cholera enterotoxin, verapamil and A23187

Net water, Na+, Cl- and HCO3- fluxes were measured in in vivo rabbit ileal loops, while mucus secretion was assessed by measuring the glycoprotein or total sialic acid secreted into the lumen, or by measuring the luminal fluid viscosity. Inoculating loops with cholera enterotoxin (CT) produced a sustained secretion of electrolytes and water, but a more transient secretion of mucus. A dose of verapamil was found which, when included in the luminal fluid, inhibited or delayed the CT-induced mucus secretion while not affecting the ongoing electrolyte and water secretion. Exposure of the ileal mucosa to the ionophore, A23187, in the presence of 2mM Ca++ resulted in a brief secretion of mucus, with no change in basal water absorption. Verapamil inhibited this A23187-induced mucus secretion. The ionophore was not effective in the absence of luminal Ca++. Thus rabbit ileum mucus secretion can be separated from electrolyte and water secretion by agents that affect Ca++ movement.     

Computational simulation of vasopressin secretion using a rat model of the water and electrolyte homeostasis

Background  

In mammals, vasopressin (AVP) is released from magnocellular neurons of the hypothalamus when osmotic pressure exceeds a fixed set-point. AVP participates to the hydromineral homeostasis (HH) by controlling water excretion at the level of the kidneys. Our current understanding of the HH and AVP secretion is the result of a vast amount of data collected over the five past decades. This experimental data was collected using a number of systems under different conditions, giving a fragmented view of the components involved in HH.     

Hepatocellular transport and secretion of biliary lipids.

Bile is the route for elimination of cholesterol from the body. Recent studies have begun to elucidate hepatocellular, molecular and physical-chemical mechanisms whereby bile salts stimulate biliary secretion of cholesterol together with phospholipids, which are enriched (up to 95%) in phosphatidylcholines. Active translocation of bile salts and phosphatidylcholines across the hepatocyte's canalicular plasma membrane provides the driving force for biliary lipid secretion. This facilitates physical-chemical interactions between detergent-like bile salt molecules and the ectoplasmic leaflet of the canalicular membrane, which result in biliary secretion of cholesterol and phosphatidylcholines as vesicles. Within the hepatocyte, separate molecular pathways function to resupply bile salts, phosphatidylcholines and cholesterol to the canalicular membrane for ongoing biliary lipid secretion.     

Effect of lithium on water and electrolyte metabolism.

Studies were performed in the rat to determine the effect of lithium on electrolyte transport in distal portions of the nephron since steep corticomedullary gradient for lithium has been demonstrated and ionic competition and/or substitution of lithium for sodium and potassium may play a role in inhibition of vasopressin-induced water transport. During the intravenous infusion of LiC1, in the absence of volume expansion and at plasma levels of 2-5 mequiv/liter of Li, maximum urine con-entration was inhibitied. Under the same conditions lithium administration impaired potassium secretion and urinary acidification and resulted in a natriuresis. These results indicate that lithium affects electrolyte transport in the same nephron segments in which the action of vasopressin is inhibitied. In addition, evidence is provided that suggests that during the chronic administration of LiC1, the sustained increase in oral intake of water and urinary flow rate results from an increase in thirst as well as reduced renal concentrating ability.     

Body water and electrolyte responses to acetazolamide in humans

Acetazolamide (ACZ), a potent carbonic anhydrase inhibitor, is a known diuretic and causal agent in metabolic acidosis. Its diuretic qualities are well established with respect to urine flow and electrolyte excretion. However, the impact of ACZ on body hydration status has not been adequately quantified. Thus, to establish the influence of ACZ treatment on body water, nine healthy males were evaluated for hydration status after clinically prescribed doses of ACZ. The drug was administered in three 250-mg oral doses 14, 8, and 2 h before determination of body water compartments. ACZ led to a significant 1.7-liter reduction in total body water (3.4%). A significant reduction in extracellular water of 3.3 liters is partitioned as the loss of total body water and a significant increase in intracellular water (1.6 liters). Venous blood pH and plasma HCO3- were significantly reduced 0.09 units and 5.9 mM, respectively, with ACZ. Plasma protein concentration was increased, but plasma osmolality did not change. Plasma Na+, K+, and Cl- concentrations were not different with ACZ, but total electrolyte content was significantly decreased 45.2, 1.17, and 44.1 meq, respectively, for all three. Urine K+, HCO3-, flow, and pH were elevated after ACZ treatment, whereas Na+ and Cl- were the same as placebo levels. In conclusion, acute clinical doses of ACZ reduce body fluid compartments, leading to a moderate isosmotic hypovolemia with an intracellular volume expansion as well as metabolic acidosis.     

Salmon calcitonin and water and electrolyte transport in rabbit ileum.

The administration of SCT, natural and synthetic, has no apparent effect on the ileal water and electrolyte transport in the rabbit. The failure of SCT to influence ileal transport of water and electrolytes in the rabbit, as it does in man, may be due to differences in the rabbit intestinal response to a foreign peptide hormone.     

Local and global calcium signals and fluid and electrolyte secretion in mouse submandibular acinar cells

Polarized Ca(2+) signals that originate at and spread from the apical pole have been shown to occur in acinar cells from lacrimal, parotid, and pancreatic glands. However, "local" Ca(2+) signals, that are restricted to the apical pole of the cell, have been previously demonstrated only in pancreatic acinar cells in which the primary function of the Ca(2+) signal is to regulate exocytosis. We show that submandibular acinar cells, in which the primary function of the Ca(2+) signal is to drive fluid and electrolyte secretion, are capable of both Ca(2+) waves and local Ca(2+) signals. The generally accepted model for fluid and electrolyte secretion requires simultaneous Ca(2+)-activation of basally located K(+) channels and apically located Cl(-) channels. Whereas a propagated cell-wide Ca(2+) signal is clearly consistent with this model, a local Ca(2+) signal is not, because there is no increase in intracellular Ca(2+) concentration at the basal pole of the cell. Our data provide the first direct demonstration, in submandibular acinar cells, of the apical and basal location of the Cl(-) and K(+) channels, respectively, and confirm that local Ca(2+) signals do not Ca(2+)-activate K(+) channels. We reevaluate the model for fluid and electrolyte secretion and demonstrate that Ca(2+)-activation of the Cl(-) channels is sufficient to voltage-activate the K(+) channels and thus demonstrate that local Ca(2+) signals are sufficient to support fluid secretion.     

The effects of alpha-methylnoradrenaline on protein and electrolyte secretion by rat submandibular and parotid glands

alpha-Methylnoradrenaline (alpha-mNA) is a potent secretagogue for the parotid and submandibular glands of rats. With regard to the parotid glands, alpha-mNA activates mainly beta-adrenoceptors. In the submandibular glands, alpha-mNA activates alpha-adrenoceptors at higher doses whereas at relatively lower doses it activates beta-adrenoceptors. alpha-mNA may not stimulate the specific alpha 2-adrenoceptors of the salivary glands of rats.     

Effects of vanadate on water and electrolyte transport in rat jejunum

The effect of vanadate (orthovanadate, VO4-) on water and ion transport was studied in rat jejunum. Water transport was tested by single-pass perfusion in vivo and ion fluxes by the Ussing-chamber technique in vitro. The results suggest that vanadate has two actions on ion and water transport: At low concentrations (10(-4) M) it causes Cl-, Na+ and water secretion by stimulation of adenylate cyclase; At higher concentrations (10(-3) and 10(-2) M) it decreases net absorption of Na+ and Cl- by inhibition of (Na+ + K+)-ATPase.     

Role of water and electrolyte influxes in anoxic plasma membrane disruption

The role of water and electrolyte influxes in anoxia-inducedplasma membrane disruption was investigated using rabbit proximal tubule suspension. The results indicated that normal proximal tubule(PT) cells have a great capacity for expanding cell volume in responseto water influx, whereas anoxia increases the susceptibility to waterinflux-induced disruption, and this was attenuated by glycine. However,resistance of anoxic plasma membranes to water influx-induced stress isnot lost, although their mechanical strength was diminished, comparedwith normoxic membranes. Anoxic membranes did not disrupt under anintra-to-extracellular osmotic difference as great as 150 mosM.Potentiating or attenuating water influx by incubating PT cells inhypotonic or hypertonic medium, respectively, during anoxia, did notaffect anoxia-induced membrane disruption. After the transmembraneelectrolyte concentration gradient was eliminated by a"intracellular" buffer or by permeabilizing the plasma membraneto molecules <4 kDa using -toxin, anoxia still caused furthermembrane disruption that was prevented by glycine or low pH. Theseresults demonstrate that 1) water ornet electrolyte influxes are probably not a primary cause foranoxia-induced membrane disruption and2) glycine could prevent the plasmamembrane disruption during anoxia independently from its effect ontransmembrane electrolyte or water influxes. The present data support abiochemical rather than a mechanical alteration of the plasma membraneas the underlying cause of membrane disruption during anoxia.