Preparation and Characterization of Alkylethoxyethanesulfonate in Superbasic System KOH-DMSO

Alkylethoxyethanesulfonate is one kind of nonionic-anionic surfactant with a polyglycol ether chain and a sulfonic group at the end of the chain. It was synthesized in a new method by using fatty alcohol-polyoxyethylene ether MOA-3, thionyl chloride and sodium isethionate as raw materials, and then the intermediate chloridepolyglycol ether MOACl-3 reacted with sodium isethionate in a superbasic system KOH-DMSO.The structures of MOA-3,MOACl-3 and alkylethoxyethanesulfonate MOASO-3 were confirmed by their IR spectrums, and the saltresistance of MOASO-3 was studied. IR analysis results indicate the intermediate and product all have the same structure with the aim compound. The saltresistance results show that MOASO-3 is compatible with NaCl aqueous solutions, when the concentration of MOASO-3 is 0.2wt%, the surfactant-water solutions were clear and transparent up 0.6wt% NaCl.

Drinking after intragastric NaCl without increase in systemic plasma osmolality in rats

Drinking after intragastric hypertonic solutions was examined to determine whether increased plasma osmolality always accompanied initiation of drinking. A 2-ml infusion through a gastric catheter was the beginning of tests in Sprague-Dawley male rats. Latency to drink was shorter and 1-h water intake was greater for increasing concentrations of NaCl (600, 1,200, and 1,800 mosmol/kg) compared with baseline (290 mosmol/kg). Although 600, 900, or 1,200 mosmol/kg NaCl elicited drinking, such infusions failed to change systemic plasma osmolality, and 900 mosmol/kg also failed to change plasma sodium, protein, renin activity, or packed cell volume at the initiation of drinking. Intragastric 900 mosmol/kg sodium bicarbonate, sodium isethionate, potassium chloride, lithium chloride, and mannitol differentially increased water intake. Total subdiaphragmatic vagotomy abolished drinking elicited by intragastric NaCl; selective gastric or hepatic vagotomy attenuated intake under some conditions. These results support the hypothesis of a vagally mediated, gastrointestinal and/or hepatic-portal, osmosensitive mechanism for initiation of drinking in advance of postprandial increases in systemic osmolality.

Chloride transport in the rat S1 proximal tubule

In vivo microperfusion was used to elucidate the modes and regulation of the powerful chloride transport system resident in the rat early (S1) proximal convoluted tubule (PCT). From a complete, glomerular ultrafiltrate-like perfusate, omission of organic solutes reduced chloride absorption by 93 peq.mm-1.min-1 (302 +/- 10 to 209 +/- 24, P < 0.001). From a high-chloride perfusate (a relatively pure NaCl solution devoid of bicarbonate and organic solutes), luminal addition of the active transport inhibitor cyanide reduced chloride absorption by 153 peq.mm-1.min-1 (632 +/- 17 to 479 +/- 9, P < 0.001). Active transport was also estimated directly as 121 +/- 4 peq.mm-1.min-1 using a solution in which sodium isethionate isosmotically replaced bicarbonate and organic solutes, preventing development of a chloride gradient. Intravenous angiotensin II caused a stimulation of chloride absorption from a high-chloride perfusate by 55 peq.mm-1.min-1 (632 +/- 17 to 687 +/- 14, P < 0.05), which was partially cyanide-sensitive (510 +/- 6 peq.mm-1.min-1). In conclusion, the components of the normal S1 PCT chloride reabsorption (approximately 300 peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following: active transport (40–50%), which can be regulated by angiotensin II; sodium-coupled organic solute transport (30%); and passive, chloride concentration gradient-driven transport (20–25%).

Splanchnic osmosensation and vasopressin: mechanisms and neural pathways

Hypertonic (2 ml, 598 mosmol/kgH2O) solutions were infused over 4 min via a stomach tube in 12 groups (n = 5-10) of conscious rats with indwelling arterial catheters. Mean changes over 4–21 min of plasma arginine vasopressin (AVP) were 6.1 +/- 0.9 for NaCl (P less than 0.01), 9.3 +/- 3.0 for LiCl (P less than 0.01), 4.5 +/- 1.3 for sodium isethionate (P less than 0.01), 2.8 +/- 0.9 for sucrose (P less than 0.025), 3.9 +/- 2.8 for mannitol (P less than 0.01), and -0.1 +/- 0.1 (SE) pg/ml for urea. The AVP responses to NaCl and sucrose were proportional to the rate of gastrointestinal absorption of radiolabeled NaCl and sucrose, respectively. The AVP response to 598 mosmol/kgH2O NaCl was attenuated by 60.6% (P less than 0.001) in rats with lesion of the side branches of the major splanchnic nerves innervating the mesentery of the upper small intestine and the portal vein area, by 34–37% (P less than 0.05) in rats with right or left splanchnic nerve lesions, and was not affected by subdiaphragmatic vagotomy. Changes in systemic plasma osmolality were small and could not explain the AVP responses. Thus splanchnic receptors are osmosensitive, are situated in the mesentery of the upper small intestine and possibly the portal vein area, and project to the spinal cord via the right and left major splanchnic nerves.

Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport

Transport inhibitor and ion substitution studies were performed using perfused, superfused preparations of the isolated rabbit juxtaglomerular apparatus to investigate transport dependency of macula densa-mediated renin secretion. In the first experimental series, tubular perfusion with a high-NaCl solution containing 10(-6) M bumetanide increased renin secretion compared with perfusion with high NaCl alone from 8.7 to 24.6 nano-Goldblatt hog units (nGU)/min. Bath addition of 10(-6) M bumetanide had no effect on renin release. The second series tested ability of luminal addition of 54 mmol/l Na or Cl salts to inhibit renin secretion, starting from a stimulated value produced by low-NaCl perfusion. Perfusion with a high-NaCl solution decreased renin secretion from 58.9 to 14.8 nGU/min, which served as a positive control. Addition of choline chloride decreased renin secretion from 42.7 to 16.6 nGU/min, and RbCl decreased renin secretion from 54.9 to 17.0 nGU/min. In contrast, addition of two different Na salts had no effect on renin release (from 41.7 to 31.6 nGU/min with sodium isethionate and from 14.1 to 13.5 nGU/min with sodium acetate). Also, in the presence of 26 mmol/l Cl, addition of 54 mmol/l Na had no effect on renin secretion (29.9-36.8 nGU/min). These data demonstrate that renin secretion is directly stimulated by luminal application of transport blockers and can be inhibited by increases in Cl concentration at the macula densa but not by changes in Na concentration. These results support the hypothesis that the initiating signal for macula densa control of renin secretion is an inverse change in transport rate via the luminal Na(+)-K(+)-2Cl- cotransporter.

Effect of sodium- or chloride-deficient medium on fast axonal transport in frog spinal nerves

Fast axonal transport of radiolabeled proteins was studied in vitro in desheathed spinal nerves from frog. The replacement of the NaCl of the medium by LiCl reduced by 58% the amount of radiolabeled proteins which accumulated at a ligature, but its replacement by choline chloride did not inhibit transport. The replacement of NaCl by sodium isethionate led to a 32% reduction in the quantity of protein-bound radioactivity at the ligature. The results suggest that Cl ions are essential to maintain fast axonal transport, and that Na+ may also be important.