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A Leaf

Publications and source records attributed to A Leaf.

At least 145 records · Page 8Linked to original sources
PubMed1978

Epithelial cell electrolytes in relation to transepithelial sodium transport across toad urinary bladder.

Aspects of the relationships between cellular composition and transepithelial sodium transport across toad urinary bladder are reviewed. Changes in cellular sodium produced by amiloride, vasopressin, aldosterone, hypoxia, ouabain, and sodium-free media are consistent with a cellular sodium transport pool. Metabolic studies suggest that this pool gains its sodium from the mucosal medium and that there is little recycling of sodium between cell and serosal medium. One-third of the cellular potassium equilibrates readily with serosal potassium. The rate of exchange of potassium is much less than the rate of sodium transport supporting the contention that sodium transport in this tissue is electrogenic. Studies with 36Cl suggest that chloride does not cross the apical cellular membranes, but exchanges with serosal chloride. Possible relationships between transepithelial sodium transport and cellular volume regulation are discussed.

Aldosterone↗
PubMed1978

Energetics of sodium transport in toad urinary bladder.

The ratio of the rate of transepithelial sodium transport, JNa, across the isolated toad urinary bladder to the simultaneously measured rate of transport-dependent metabolism, JsbCO2, has been measured as a function of the transepithelial electrical voltage, deltapsi. The ratio remains constant with a mean value of 18 to 20 over the range of imposed voltages of 0 to +70 mV. With increasing hyperpolarization of the bladder, JNa decreases and the calculated electromotive force or apparent "ENa" of the sodium pump increases. From thermodynamic and kinetic arguments it is shown that the apparent "ENa" approaches the maximal electrochemical potential gradient, ENa, against which sodium can be transported by this tissue only when JNa approximately 0. At this unique condition F ENa (in which F is the Faraday constant) is the maximal free energy of the chemical reaction driving sodium transport and thus equal to the maximal extramitochondrial phosphorylation potential and the maximal free energy of the mitochondrial respiratory chain within the transporting cells.

Animals↗
PubMed1978

The sodium transport pool.

The sodium transport pool in epithelial cells represents sodium involved in active transport across the epithelium. There has been much controversy about the size of such a pool and even about its existence. Techniques for estimating the size of this pool are described. By analysis of toad bladder epithelial cells scraped from hemibladders mounted in chambers under a variety of conditions it has proved possible to detect and to quantify a sodium transport pool. Only about 20 percent of non-inulin space sodium measured flame photometrically is contained in this pool. This represents the total sodium entering cells from the mucosal medium, is in good agreement with the cellular sodium measured by the electron microprobe, and averages some 10-16 mmol/kg tissue H2O. Measurements of the pool in other tissues are considered.

Animals↗
PubMed1978

Effect of exogenous and endogenous angiotensin II in the isolated perfused rat kidney.

Rat kidneys were perfused with an artificial solution at constant pressure. The infusion of angiotensin II (AII) (1.5--6 ng min-1) reduced renal perfusate flow (RPF) from 36.6 +/- 2.4 to 19.3 +/- 1.4 ml min-1 (P less than 0.001) (n = 13); GFR rose from 0.48 +/- 0.06 to 0.63 +/- 0.04 ml min-1 (P less than 0.05), and filtration fraction (FF) rose accordingly from 0.015 +/- 0.002 to 0.033 +/- 0.003 (P greater than 0.01). The same results were obtained with purified renin substrate (synthetic tetradecapeptide, 100 ng min-1, n = 8); RPF fell from 31.5 +/- 2.9 to 17.2 +/- 2 ml min-1 (P less than 0.001), GFR rose from 0.36 +/- 0.05 to 0.51 +/- 0.04 ml min-1 (P less than 0.05), and FF increased from 0.021 +/- 0.002 to 0.034 +/- 0.006 (P less than 0.01). The effects of renin substrate were completely prevented by the converting enzyme inhibitor SQ 20,881 (3 X 10(-5) M). In another six experiments the effects of renin substrate at the same dose were fully reversed by addition of the analogue [Sar1,Ala8]AII. We interpret these findings to indicate that both exogenous and endogenous AII produce preferential vasoconstriction of the efferent arteriole, increasing the driving force for ultrafiltration and thereby maintaining or increasing GFR in the face of a reduced plasma flow.

Angiotensin II↗
PubMed1977

Metabolic cost of sodium transport in toad urinary bladder.

The metabolic cost of active sodium transport was determined in toad bladder at different gradients of transepithelial potential. Deltapsi, by continuous and simultaneous measurements of CO2 production and of transepithelial electric current. Amiloride was used to block active sodium transport in order to assess the nontransport-linked, basal, production of CO2 and the passive permeability of the tissue. From these determinations active sodium transport, Jna, and suprabasal CO2 production, Jsb CO2, were calculated. Since large transients in Jna and Jsb CO2 frequently accompanied any abrupt change in deltapsi, steady state conditions were carefully defined. Some 20 to 40 min were required after a change in deltapsi before steady state of transport activity and of CO2 production were achieved. The metabolic cost of sodium transport proved to be the same whether the bladder expended energy moving sodium against a transepithelial electrical potential grandient of +50 mV or whether sodium was being pulled through "the active transport pathway" by an electrical gradient of -50 mV. In both cases the value of the ratio Jna/Jsb CO2 averaged some 20 sodium ions transported per molecule of CO2 produced. When the Na pump was blocked by 10(-2) M ouabain, the perturbations of the transepithelial electrical potential did not elicit changes of Jna nor, consequently of Jsb CO2. The independence of the ratio Jna/Jsb CO2 from deltapsi over the range+/-50 mV indicates a high degree of coupling between active sodium transport and metabolism.

Amiloride↗
PubMed1976

Metabolic evidence that serosal sodium does not recycle through the active transepithelial transport pathway of toad bladder.

The possibility that sodium from the serosal bathing medium "back diffuses" into the active sodium transport pool within the mucosal epithelial cell of the isolated toad bladder was examined by determining the effect on the metabolism of the tissue of removing sodium from the serosal medium. It was expected that if recycling of serosal sodium did occur through the active transepithelial transport pathway of the isolated toad bladder, removal of sodium from the serosal medium would reduce the rate of CO2 production by the tissue and enhance of stoichiometric ratio of sodium ions transported across the bladder per molecula of sodium transport dependent CO2 produced simultaneously by the bladder (JNa/JCO2). The data revealed no significant change in this ratio (17.19 with serosal sodium and 16.13 after replacing serosal sodium with choline). Further, when transepithelial sodium transport was inhibited (a) by adding amiloride to the mucosal medium, or (b) by removing sodium from the mucosal medium, subsequent removal of sodium from the serosal medium, or (c) addition of ouabain failed to depress the basal rate of CO2 production by the bladder [(a)rate of basal, nontransport related, CO2 production (JbCO2) equals 1.54 +/- 0.52 with serosal sodium and 1.54 +/- 0.37 without serosal sodium; (b) Jb CO2 equals 2.18 +/- 0.21 with serosal sodium and 2.09 +/- 0.21 without serosal sodium; (c) 1.14 +/- 0.26 without ouabain and 1.13 +/- 0.25 with ouabain; unite of JbCO2 are nmoles mg d.w.-1 min-1]. The results support the hypothesis that little, if any, recycling of serosal sodium occurs in the total bladder.

Amiloride↗
PubMed1976

The protective effect of hyperosmotic mannitol in myocardial ischemia and necrosis.

Morphologic and hemodynamic changes that occur following coronary occlusion are examined. The effectiveness of hyperosmotic mannitol in lessening the extent of myocardial damage is assessed and mechanisms for its action discussed. Forty and 60 min of coronary vascular occlusion followed by 15 and 45 min of reflow were associated with a persistence of ischemia following reflow of blood, as established by infusions of silastic into the aortic root. Electron microscopic studies demonstrated myocardial and endothelial cell swelling at the end of the reflow period. The process of cell swelling appeared to be initiated during the period of arterial occlusion. This cell swelling was reduced by elevation of serum osmolality by 30-40 mOsm above control with the administration of mannitol during and following occlusion. There was an associated 40-50% reduction of vascular resistance following occlusion if mannitol was administered. In addition, the extent of necrosis, which was widespread in untreated hearts 12 hours after occlusion, was strikingly less in the hearts of dogs which received mannitol. Thus, in ischemic myocardium, elevation of osmolality by mannitol reduces myocardial necrosis, probably through its restoration of normal cell volume.

Animals↗
PubMed1976

Fuller Albright.

Explore the source record for details and available documents.

Diet↗
PubMed1976

Effects of hyperosmotic mannitol in reducing ischemic cell swelling and minimizing myocardial necrosis.

Impaired metabolism interferes with the active extrusion of intracellular sodium and results in intracellular edema. In the brain and regionally in the kidney, elevation of extracellular osmolality is accompanied by a reduction of ischemic cell swelling and improvement of reflow of blood after arterial occlusion. Studies were therefore performed to examine the effect of elevation of extracellular osmolality on ischemic myocardial physiology and by morphologic examination on the extent of acute injury and subsequent necrosis. Under conditions of controlled hemodynamics, administration of hyperosmotic mannitol resulted in improvement of function of the canine heart with regional ischemia, a lessening of the extent of ischemic injury assessed by electrocardiographic ST segment mapping, and improved total and collateral blood flow. Metabolic studies under conditions of controlled hemodynamics revealed that hyperosmotic mannitol reduced the myocardial oxygen requirement of the ischemic heart. Mannitol dilated large collateral conductance vessels in addition to improving blood flow through the region of myocardial ischemia. Under conditions of ischemia induced by a prolonged reduction in coronary perfusion, hyperosmotic mannitol attenuated the progressive rise in vascular resistance. Direct morphologic examination of areas of myocardium subjected to total interruption of blood flow followed by reflow of blood revealed swelling of both myocardial and capillary endothelial cells early during the reflow period. The extent of swelling was substantially reduced with elevation of the extracellular osmolality with mannitol. Simarilty, osmolality elevation strikingly reduced the extent of eventual myocardial necrosis following prolonged periods of reflow of blood.

Animals↗
PubMed1975

Coupling of sodium transport to respiration in the toad bladder.

Energy expenditure and transepithelial sodium transport were measured continuously and simultaneously from isolated urinary bladders of the Dominican toad, Bufo marinus. Sodium transport was measured as the short-circuit current and CO2 produced by the bladder was measured conductometrically by the method of Maffly. The rates of sodium transport and CO2 productions were linearly related. The slope of the regression of sodium transport on CO2 production, dJNa/dJCO2, was found to be quite similar in paired half bladders but to differ significantly between bladders from different toads. Thus, in this preparation there appears to be no unique stoichiometric ratio characterizing sodium transport and metabolism and past efforts to arrive at such a value by averaging results obtained from different animals do not seem warranted. The CO2 production by the isolated bladder which is unrelated to sodium transport was determined by two means: 1) extrapolating the regression of JNa on JCO2 to JNa equals O, and 2) measuring CO2 production with sodium transport suppressed by removal of all sodium from the mucosal bathing medium. The two methods gave values which were in close agreement in each preparationmthis suggests that metabolism which supports nontransport activities in this tissue cannot be recruited to support the energy requirement of sodium transport and vice versa.

Animals↗
PubMed1975

The sodium transport pool in toad urinary bladder epithelial cells.

The sodium which equilibrates with 24-Na in epithelial cells of toad urinary bladders has been determined. With sodium Ringer's bathing both mucosal and serosal surfaces, 24-Na in the mucosal medium equilibrated with about 35 mmoles cellular sodium/kg cellular dry weight, representing about 20% of the total cellular sodium determined flame photometrically; 24-Na in the serosal medium equilibrated with 120 mmoles cellular sodium/kg cellular dry weight, about 80% of the total cellular sodium. With 24-Na in both media all cellular sodium was labeled within 30 min. In the absence of serosal sodium, total cellular sodium and that sodium which equilibrated with mucosal 24-Na in sodium Ringer's were both similar to the cellular sodium of mucosal origin which had been determined in epithelial cells exposed on both surfaces to sodium Ringer's. Sodium-free mucosal medium, and sodium Ringer's containing amiloride 10-4 or 10-3 M in the mucosal medium, both virtually completely inhibited transepithelial sodium transport. But, whereas the cellular sodium of mucosal origin fell to only 2 mmoles/kg cellular dry weight with sodium-free mucosal medium, an appreciable labeling of cellular sodium was found whether amiloride was present before, or only after, exposure of tissue to mucosal 24-Na. Rapid washing of the mucosal surface of hemibladders just before removal of epithelial cells for analysis removed most of this sodium labeled in the presence of amiloride, suggesting that the cellular sodium of mucosal origin consists of at least two fractions with only about two-thirds truly intracellular. The sodium transport pool measured directly in these experiments is appreciably smaller than any previous estimates of pool size all of which have been obtained by indirect techniques involving use of whole hemibladders rather than epithelial cells alone.

Amiloride↗
PubMed1975

Some effects of ouabain on cellular ions and water in epithelial cells of toad urinary bladder.

Transepithelial sodium transport was virtually abolished when toad urinary hemibladders, mounted in chambers and short-circuited, were exposed on their serosal surface to ouabain, 10-2 M,for 60 minutes. Epithelial cells scraped from such hemibladders gained sodium and lost an equal quantity of potassium when compared with controls not exposed to cardiac glycoside. Their total cellular cation content, chloride content and water content were unchanged. Experiments in which 24-Na, amiloride, or sodium-free mucosal solutions were used, revealed that a large, though variable, percentage of the sodium gained by cells exposed to oubain, came from the mucosal medium, a finding consistent with the model of passive sodium entry from the mucosal medium followed by active sodium extrusion to the serosa. The oubain-insensitive maintenance of cellular volume which was observed did not depend upon transepithelial sodium transport which had been virtually completely inhibited by ouabain. Neither did the maintenance of a normal cellular potassium content depend upon transepithelial sodium transport, for cellular potassium was unaffected when the mucosal medium was sodium-free or when it contained sufficient amiloride, 10-3 M, to virtually abolish such transport.

Amiloride↗