Active transport of Fe59 by everted segments of rat duodenum

1960 ◽  
Vol 198 (3) ◽  
pp. 609-613 ◽  
Author(s):  
Eugene B. Dowdle ◽  
David Schachter ◽  
Harris Schenker
Keyword(s):  
Small Intestine ◽  
Active Transport ◽  
Transport Process ◽  
Transport Mechanism ◽  
Concentration Gradients ◽  
Active Transport Mechanism ◽  
Proximal Small Intestine ◽  
Rat Duodenum ◽  
Active Transport Process

Everted gut sacs prepared from segments of the proximal small intestine of rats transport Fe59 from the mucosal to the serosal surfaces against concentration gradients in vitro. The active transport mechanism is dependent upon oxidative metabolism and the generation of phosphate-bond energy, and is limited in capacity. The active transport process is maximal in the region of the small intestine immediately distal to the pylorus and diminishes with more distal segments of the gut. Addition of ascorbic acid to the incubation medium markedly increases the active transport of Fe59 in vitro.

Active transport of Ca45 by the small intestine and its dependence on vitamin D

1959 ◽  
Vol 196 (2) ◽  
pp. 357-362 ◽  
Author(s):  
David Schachter ◽  
Samuel M. Rosen
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Active Transport ◽  
Transport Mechanism ◽  
Calcium Citrate ◽  
Concentration Gradients ◽  
Citrate Complex ◽  
Active Transport Mechanism ◽  
Proximal Small Intestine

Everted gut-sacs prepared from segments of the proximal small intestine of young rabbits, rats and guinea pigs transport Ca45 in vitro from the mucosal to the serosal surfaces against concentration gradients. The active transport mechanism is limited in capacity, is dependent on oxidative phosphorylation, and appears to be relatively specific for Ca++ and Mg++ in contrast to Sr++ and Ba++. Vitamin D deprivation in rabbits and rats markedly impairs the capacity for active Ca45 transport in vitro. The vitamin thus has an effect directly on the upper small intestine. Neither the active Ca45 transport nor the effect of vitamin D on the transport can be explained by an accumulation of citrate and the formation of the calcium-citrate complex.

Active transport of calcium by the small intestine of the rat

1960 ◽  
Vol 198 (2) ◽  
pp. 263-268 ◽  
Author(s):  
David Schachter ◽  
Eugene B. Dowdle ◽  
Harris Schenker
Keyword(s):  
Small Intestine ◽  
Active Transport ◽  
Transport Mechanism ◽  
Cation Transport ◽  
Maximal Rate ◽  
Active Transport Mechanism ◽  
Serosal Surface ◽  
Proximal Small Intestine ◽  
Active Transfer

The rates of active transport of calcium in vitro by everted gut-sacs prepared from the proximal small intestine of the rat have been quantified and expressed in absolute units. A maximal rate of transport has been measured. The bulk of the calcium transferred to the serosal surface of the gut-sac is ionized calcium, suggesting that the process is an active cation transport mechanism. The active transfer is relatively specific for Ca++, and no significant accumulation of Mg++, Sr++, Ba++ or K+ in the fluid bathing the serosal surface could be demonstrated. The active transport of calcium in vitro is greater with gut-sacs from growing than from older rats, and it is greater with gut-sacs from pregnant than from nonpregnant rats. The results suggest that the active transport mechanism can increase the intestinal absorption of calcium facultatively to meet the needs of the organism.

Active transport of calcium by intestine: effects of dietary calcium

1961 ◽  
Vol 200 (6) ◽  
pp. 1256-1262 ◽  
Author(s):  
Daniel V. Kimberg ◽  
David Schachter ◽  
Harris Schenker
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Active Transport ◽  
Adaptive Response ◽  
Transport Mechanism ◽  
Concentration Gradients ◽  
Active Transport Mechanism ◽  
Entire Small Intestine ◽  
Young Rat

The small intestine of the rat responds facultatively to a diet low in Ca by increasing the active transport of the cation. The effects of calcium deprivation were studied with everted gut sacs and with duodenal slices in vitro, and the experiments demonstrate that following this stimulus almost the entire small intestine of a young rat can transfer calcium from the mucosa to the serosa against concentration gradients. The active transport is maximal in duodenum, less in ileum, and least in the mid small intestine. Following the low-Ca diet, duodenal gut sacs transport Sr89 against concentration gradients, although strontium is transferred much less readily than is calcium. Vitamin D is required for the adaptive response of the active transport in duodenum and ileum. Younger rats respond to Ca deprivation earlier and more markedly than older animals. Neither thyroparathyroidectomy, hypophysectomy, or adrenalectomy prevent response to the low-Ca diet, although these ablations do affect the active transport mechanism in rats on a given diet.

The Influx of Uric Acid and other Purines into Everted Jejunal Sacs of the Rat and Hamster

1975 ◽  
Vol 53 (1) ◽  
pp. 113-119 ◽  
Author(s):  
A. H. Khan ◽  
S. Wilson ◽  
J. C. Crawhall
Keyword(s):  
Uric Acid ◽  
Active Transport ◽  
Concentration Gradient ◽  
Incubation Medium ◽  
Transport Mechanism ◽  
Concentration Gradients ◽  
Bicarbonate Buffer ◽  
Active Transport Mechanism ◽  
Everted Jejunal Sacs

The in vitro transport of [2-14C]uric acid, [8-14C]hypoxanthine, and [8-14C]xanthine, each dissolved in Krebs–Ringer bicarbonate buffer, was studied with everted jejunal sacs from rat and hamster. No evidence could be obtained for the development of a concentration gradient between the intracellular fluid and the incubation medium or between the sac contents and the incubation medium, for any of the three oxypurines. Inhibitors of active transport, such as anaerobiosis or dinitrophenol, had no significant effect on the rate of transport. A large percentage of hypoxanthine and xanthine was oxidized to uric acid in the sac-wall homogenate, sac contents, and incubation medium during the course of the incubation. This oxidation could be prevented by addition of allopurinol (3 mM) to the incubation medium, but concentration gradients were still not obtained. No active transport mechanism could be demonstrated for uric acid, hypoxanthine, or xanthine in rat or hamster jejunum.

Ionic regulation of Na absorption in proximal colon: cation inhibition of electroneutral Na absorption

1987 ◽  
Vol 252 (1) ◽  
pp. G100-G108
Author(s):  
J. H. Sellin ◽  
R. De Soignie
Keyword(s):  
Linear Function ◽  
Active Transport ◽  
Transport Process ◽  
Proximal Colon ◽  
High Rate ◽  
Ionic Regulation ◽  
Diffusional Flux ◽  
Active Transport Process

Active Na absorption (JNanet) in rabbit proximal colon in vitro is paradoxically stimulated as [Na] in the bathing media is lowered with constant osmolarity. At 140 mM [Na]o, JNanet is -0.6 +/- 0.4 mueq X cm-2 X h-1, whereas at 50 mM [Na]o JNanet is 5.0 +/- 0.7 mueq X cm-2 X h-1, P less than 0.01. JNas----m is a linear function of [Na]o, suggesting a diffusional flux. JNam----s increases almost linearly from 0 to 50 mM [Na]o but then plateaus and actually decreases from 50 to 140 mM [Na]o, consistent with inhibition of an active transport process. Both lithium and Na are equally effective inhibitors of JNanet, whereas choline and mannitol do not block the high rate of JNanet observed in decreased [Na]o. Either gluconate or proprionate replacement of Cl inhibits JNanet. Removal of K or HCO3 does not alter Na absorption. JNanet at lowered [Na]o is electrically silent and is accompanied by increased Cl absorption; it is inhibited by 10(-3) M amiloride and 10(-3) M theophylline but not by 10(-4) M bumetanide. Epinephrine is equally effective at stimulating Na absorption at 50 and 140 mM [Na]; yohimbine does not inhibit JNanet at 50 mM [Na]o. Na gradient experiments are consistent with a predominantly serosal effect of the decreased [Na]o. These results suggest that Na absorption in rabbit proximal colon in vitro is stimulated by decreased [Na]; the effect is cation specific, both Na and Li blocking the stimulatory effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Active transport of calcium by intestine: action and bio-assay of vitamin D

1961 ◽  
Vol 200 (6) ◽  
pp. 1263-1271 ◽  
Author(s):  
David Schachter ◽  
Daniel V. Kimberg ◽  
Harris Schenker
Keyword(s):  
Vitamin D ◽  
Active Transport ◽  
Calcium Transport ◽  
Transport Mechanism ◽  
Simple Diffusion ◽  
Active Mechanism ◽  
Active Transport Mechanism ◽  
Small Doses ◽  
Bio Assay

Vitamin D is required for the active transport of calcium in vitro. Small doses of vitamins D2 and D3 restore the mechanism in depleted rats, and this provides a sensitive bio-assay for the vitamin, independent of an antirachitic effect. Vitamin D influences calcium transfer in all segments of the small intestine, and maximal increments are observed in the duodenum. The effect of vitamin D requires oxidative metabolism in vitro, is maximal where active transport is maximal, and the sterol increases the maximal rates of active transport of calcium. Consequently, vitamin D influences calcium transport by affecting primarily the active mechanism rather than by simple diffusion. Experiments with various monosaccharides demonstrate that two distinct steps are involved in the active transport mechanism in duodenum. Vitamin D is required for both of the steps.

Active transport of iron by intestine: effects of oral iron and pregnancy

1962 ◽  
Vol 203 (1) ◽  
pp. 81-86 ◽  
Author(s):  
James G. Manis ◽  
David Schachter
Keyword(s):  
Single Dose ◽  
Active Transport ◽  
Transport Mechanism ◽  
Iron Absorption ◽  
Late Pregnancy ◽  
Cellular Processes ◽  
Active Transport Mechanism ◽  
Mucosal Uptake

The active transport of iron has been studied further with everted gut sacs and loops of duodenum in the rat. The two-step absorptive mechanism appears to be one of the cellular processes which regulates iron absorption. A single dose of iron by mouth decreases both the net mucosal uptake and the net serosal transfer of iron, as studied with gut sacs in vitro. As little as 0.1 mg Fe is effective; the inhibition observed with 4.0 mg Fe persisted for approximately 17 hr. The reduction in transport appears to result, in part at least, from a direct effect of Fe on the intestine. The active transport mechanism also responds adaptively to the level of Fe in the diet. Late pregnancy increases the Fe transport, as observed with gut sacs in vitro and duodenal loops in vivo, and the effect is primarily on the serosal transfer step.

Active transport of lead-210 by everted segments of rat duodenum

1984 ◽  
Vol 247 (2) ◽  
pp. G193-G198
Author(s):  
J. C. Barton
Keyword(s):  
Active Transport ◽  
Sodium Azide ◽  
Sodium Cyanide ◽  
Metabolic Inhibitors ◽  
Concentration Gradients ◽  
Rat Duodenum ◽  
Lead 210 ◽  
Mucosal Uptake ◽  
Relative Inhibition

Everted gut sacs prepared from rat duodenum can transfer 210Pb from mucosal to serosal surfaces against concentration gradients in vitro. The mechanism requires oxygen and is significantly inhibited by sodium azide, sodium iodoacetate, 2,4-dinitrophenol, sodium cyanide, and sodium fluoride. Lack of oxygen or the presence of metabolic inhibitors produced greater relative inhibition of net serosal transfer but greater absolute decrements of net mucosal uptake. Treatment of rats prior to sac preparation with either intravenous FeCl2 or endotoxin, or the addition of FeCl2 to the mucosal medium, selectively inhibited net serosal transfer. Net mucosal uptake and net serosal transfer were significantly negatively correlated with animal weight. Jejunal or ileal sacs did not actively transport 210Pb.

EFFECTS OF INTRA-ARTERIAL PERFUSIONS ON ELECTRICAL ACTIVITY AND ELECTROLYTE CONTENTS OF DOG SMALL INTESTINE

1965 ◽  
Vol 43 (4) ◽  
pp. 551-577 ◽  
Author(s):  
E. E. Daniel
Keyword(s):  
Small Intestine ◽  
Active Transport ◽  
Action Potentials ◽  
Transport Process ◽  
Longitudinal Muscle ◽  
Lithium Ion ◽  
Slow Waves ◽  
Sodium Ion ◽  
Intestinal Slow Waves ◽  
Active Transport Process

The mechanisms underlying the periodic depolarizations (slow waves) in longitudinal muscle of the small intestine were studied in vivo in dogs by means of intra-arterial perfusions of solutions with altered electrolyte concentrations or with added metabolic inhibitors. Perfusion of solutions containing reduced sodium, potassium, or chloride concentrations markedly altered electrolyte concentrations in intestinal muscle but did not necessarily alter intestinal slow waves seriously. However, when lithium ion was substituted for sodium ion serious depression of slow waves occurred. This was also found with ouabain, NaF, and Na2EDTA, substances which, like lithium, are believed to inhibit the active transport process directly. Iodoacetate and dinitrophenol had little depressant effect on intestinal slow waves in amounts sufficient to cause downhill ion movements. NaCN or 1,10-phenanthroline depressed slow waves, but the effect of NaCN was largely prevented by prior reserpinization of the dog. The depressant effects of lithium ion, ouabain, NaF, and Na2EDTA were diminished but not abolished by reserpinization. It was concluded that lower amounts of inhibitors of the active transport process abolished intestinal slow waves by causing the release of catecholamines from intrinsic nerve endings in the intestine. The released catecholamines then depressed slow waves. In higher amounts, inhibitors of the active transport process depressed intestinal slow waves by a direct action, unaffected by reserpinization. Intestinal slow waves were therefore postulated to originate from the oscillatory activity of an electrogenic sodium pump.Perfusates with elevated sodium or potassium concentration initiated action potentials in intestinal longitudinal muscle. These action potentials were blocked by atropine and hexamethonium. In reserpinized animals, Na2EDTA or large amounts of ouabain also initiated action potentials which were stopped or prevented by atropine. It was postulated that all these procedures caused acetylcholine release from intrinsic parasympathetic nerves and that the common mechanism was displacement of mediator by net entrance of sodium ion. This same mechanism may also have accounted for the release of catecholamines from intrinsic sympathetic nerves mentioned above.

Sign in / Sign up

Export Citation Format

Share Document