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.     

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.     

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.     

The hypothermic hamster brain: Its water and electrolyte content and perfusion

The data suggest that cold swelling of the brain does not occur in hypothermic hamsters for up to 48 hr or in the hypothermic rat for 2 hr. It may be possible that the adaptation of the Na⁺,K⁺-activated ATPase system as well as lipid changes occurs during the 6- to 8-hr induction period of hypothermia in the hamster. The absence of swelling in the rat, a species which does not hibernate, may be due to both the lack of hypercapnia and the brevity of the hypothermic period. It is noteworthy that in the hamster the distribution of cardiac output to the brain and the respiratory centers of the brain system is unaffected by hypothermia of up to 18 hr. Actual perfusion is, however, dramatically reduced. The data suggest that the helium-cold hypothermic hamster retains the ability to maintain solute gradients in hypothermia, and that hypothermic death is not due to an increase in cerebral water content or in the percentage of cardiac output received by the brain.     

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.