scholarly journals Possible Active Transport Mechanism in Pharmacokinetics of Flunixin-Meglumin in Rabbits.

2001 ◽  
Vol 63 (8) ◽  
pp. 885-888 ◽  
Author(s):  
Yoshie MIYAZAKI ◽  
Yoshihiro HORII ◽  
Naohiro IKENAGA ◽  
Minoru SHIMODA ◽  
Eiichi KOKUE
Keyword(s):  
Active Transport ◽  
Transport Mechanism ◽  
Active Transport Mechanism

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.

Vasoactive intestinal peptide stimulates alkali excretion in turtle urinary bladder

1987 ◽  
Vol 252 (4) ◽  
pp. C428-C435 ◽  
Author(s):  
J. H. Durham ◽  
C. Matons ◽  
W. A. Brodsky
Keyword(s):  
Urinary Bladder ◽  
Cyclic Amp ◽  
Vasoactive Intestinal Peptide ◽  
Active Transport ◽  
Transport Mechanism ◽  
Phosphodiesterase Inhibitor ◽  
Camp Analog ◽  
Active Transport Mechanism

The turtle urinary bladder possesses an active transport mechanism for the electrogenic secretion of alkali. This process is independent of exogenous Cl and Na, induced by cyclic AMP (cAMP), and potentiated in bladders from NaHCO3-loaded (alkalotic) turtles. In the present study, it is shown that the serosal addition of vasoactive intestinal peptide (VIP) induces rapidly developing parallel increases in alkali secretion and in the short-circuiting current carried by this secretion. The VIP-induced increment in alkali secretion is greater in the presence than in the absence of an exogenously added phosphodiesterase inhibitor. Additions of a cAMP analog subsequent to the VIP-induced alkali secretion fail to induce any further increase in alkalinization. These results provide evidence for the action of VIP as a hormonal up regulator of alkali excretion in the turtle urinary bladder.

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.

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.

Endothelium and Serotonin Transport

1975 ◽  
Author(s):  
D. Shepro ◽  
H. B. Hechtman ◽  
F. A. Belamarich
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Active Transport ◽  
Pulmonary Circulation ◽  
Transport Mechanism ◽  
Metabolic Inhibitors ◽  
Pulmonary Insufficiency ◽  
Active Transport Mechanism ◽  
Serotonin Transport ◽  
5 Ht Uptake

The transport of serotonin (5-HT) by endothelial cells (EC) was measured in isolated blood vessels, freshly harvested cells and in the isolated dog lung. In addition cultured bovine aortic EC were used to measure 5-HT transport when they reached confluency (7 days). The EC in all preparations removed 14C-5-HT even in the presence of iproniazid (5 × 10−4 M). In freshly isolated EC and cultured EC Imipramine (10−4 M) reduced uptake. Metabolic inhibitors, cold (4° C), ouabain (10−5M) also reduced uptake suggesting that 5-HT uptake may be coupled to an active transport mechanism. Six analogues of 5-HT only reduce uptake in freshly isolated EC. Lungs that showed variable degrees of pulmonary insufficiency did not remove 5-HT despite significant platelet entrapment. These results indicate that: (1) 5-HT transport is a function of all EC and not unique to the pulmonary circulation; (2) uptake of 5-HT by EC is coupled to an active transport mechanism; (3) a model using cultured EC to measure 5-HT transport is comparable to other systems, e.g. platelets and brain; (4) EC damage results in a loss of 5-HT uptake by the lung.

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.

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