PubMed Health⌕ Search

Biomedical subjects

K Turnheim

Publications and source records attributed to K Turnheim.

At least 55 records · Page 3Linked to original sources
PubMed1981

Modification of cation permeability of rabbit descending colon by sulphydryl reagents.

1. Addition of the organic mercurials mersalyl, p-chloromercuribenzoate, and p-chloromercuribenzene sulphonate to the Ringer solution (140 mM-Na) bathing the luminal side of isolated epithelia of rabbit descending colon increases short-circuit current (Isc) and tissue conductance (Gt) when the spontaneous Isc is below 2-3 muequiv/cm2 hr. 2. The stimulation of Isc by mersalyl is due to an increase in Na absorption, simultaneously K secretion is induced, whereas Cl absorption is not affected. 3. Mersalyl inhibits Isc at Na concentrations below 50 mM. The Na concentration at which Isc is half-maximal (KNa) is shifted by mersalyl from 25 to 133 mM. The overshoot in Isc to a peak volume of 5 muequiv/cm2 hr observed when Na-depleted tissues are suddenly exposed to Na is markedly depressed by mersalyl. 4. Mersalyl inhibits non-competitively the blocking effect of amiloride on Isc. Both the stimulation of Isc and the inhibition of the amiloride effect by mersalyl have the same time course (half-time of the effects 30-40 min) and similar concentration-response curve (half-maximal effects with 2.0-2.6 x 10(-4) M), indicating a common mechanism. 5. The mersalyl effects on Isc and on the amiloride action are only partially reversed by dimercaptopropanol. p-Chloromercuribenzoate conjugated with dextran (mol. wt. 10,000) elicited the same effects as mersalyl. 6. The stoichiometry of the mersalyl-amiloride interaction, estimated by use of the Hill plot, is 1:1; a Hill coefficient of 1 was also obtained for the stimulating effect of mersalyl on Isc. 7. It is concluded that one sulphydryl group per luminal Na entry site controls both its Na conductance and cation selectivity. Titration of these sulphydryl groups by organic mercurials appear to fix the conductance of the luminal Na entry mechanism in a submaximal position and prevent its modulation by amiloride or variations in intra- and/or extracellular Na concentrations.

Amiloride↗
PubMed1980

[Basics of intestinal electrolyte transport (author's transl)].

In the small and large intestine Na and Cl are absorbed via active transport systems, whereas K appears to distribute passively between the lumen and the blood side of the epithelium. Three types of Na influx mechanisms across the luminal cell membrane of the epithelium may be distinguished: 1. In the gall bladder and the small intestine Na and Cl influx are coupled in an obligatory one for one fashion, hence this influx mechanism is electrically neutral. This coupled NaCl uptake process in the luminal cell membrane is inhibited by a rise in intracellular cAMP levels. 2. In the colon Na influx is not dependent on Cl influx. Due to the partition of cations and anions the Na uptake process is electrogenic, i.e. the electrical potential difference across the luminal cell membrane is decreased. This type of Na influx is blocked by the diuretic amiloride and enhanced by aldosterone. The electrogenic Na influx mechanism is also present in the ileum together with the neutral NaCl influx mechanism. Active Cl absorption in the colon is electrically neutral, most likely Cl is exchanged for HCO3 at the luminal membrane. Stimuli which increase cellular cAMP or Ca cause electrogenic Cl secretion. 3. In the ileum exists an additional Na influx mechanism which is dependent on the presence of certain sugars (glucose) or amino acids (alanine) on the luminal side of the epithelium. This process is inhibited by phlorizin. The finding of glucose-stimulated Na absorption has proven to be therapeutically useful: the rate of intestinal fluid loss can be decreased in certain forms of diarrhea by oral administration of electrolyte solutions containing glucose.

Animals↗
PubMed1980

Active secretion of hypoxanthine and xanthine by guinea pig jejunum in vitro.

Isolated epithelium of guinea pig jejunum secretes hypoxanthine and xanthine by a transport process that is capable of uphill transport and dependent on metabolic energy supply. Unidirectional influx of hypoxanthine across both the luminal and the contraluminal cell membrane appears to be saturable; influx across the contraluminal membrane is inhibited by 2,4-dinitrophenol (DNP). Efflux across the luminal membrane is diminished by DNP; efflux across the contraluminal membrane is increased by DNP. This evidence suggests the existence of a mediated transport system both in the luminal and the contraluminal cell membrane. Additionally, intracellular metabolism of hypoxanthine seems to regulate transepithelial permeation: increased hypoxanthine salvage by the phosphoribosyltransferase reduces the rate of secretion. However, the incorporation of hypoxanthine into the nucleotides is limited when the hypoxanthine is added to the luminal side of the epithelium, and the permeation rate in the absorptive direction is not markedly influenced by the rate of hypoxanthine salvage. These findings are a further example of the functional orientation of the jejunal epithelial cells with respect to enzymic activity and transepithelial transport properties.

Animals↗
PubMed1980

[Inhibition of sodium transport in the colon by the diuretic amiloride (author's transl)].

In isolated epithelia of rabbit descending colon the short-circuit current (Isc) is solely attributable to net transepithelial Na-transport, which in turn is identical with the unidirectional Na-influx across the luminal cell membranes. Amiloride blocks Isc by inhibiting luminal Na-influx into the cells. The type of inhibition exerted by amiloride in this tissue has to be termed mixed-type, since both the affinity of Na to its transport system and the maximal transport capacity are reduced. Na, on the other hand, is a competitive antagonist of the amiloride effect with a Ki of 136 mM; therefore KA, the amiloride-concentration at which the amiloride-effect is half-maximal, is increased from 0.14 microM at 5 mM Na in the incubation medium to 0.29 microM at 140 mM Na. It is conceivable that an "amiloride-like" action of Na may be responsible for the saturability of luminal Na-influx with increasing Na-concentrations.

Amiloride↗
PubMed1978

pH and temperature dependence of adenosine uptake in human erythrocytes.

Kinetic analysis of the saturable adenosine uptake in human erythrocytes suggests the existence of two saturable components, distinguished by different Km values (1.4 and 260 micron, respectively, at pH 7.4 and 25 degrees C). Both components were abolished by p-nitrobenzylthioguanosine or dipyridamole. Total uptake was significantly higher at pH 8 than at pH 7 at adenosine concentrations above 2 micron. The increase in uptake at the higher pH was brought about mainly by an increase in the maximum rate of transport of the low-affinity uptake system. With rising temperature the Km and the V of both uptake components increased. No transition temperature was observed between 12 and 37 degrees C.

Adenosine↗
PubMed1978

Intracellular chloride activities in rabbit gallbladder: direct evidence for the role of the sodium-gradient in energizing "uphill" chloride transport.

Intracellular chloride activities, (Cl)c, in rabbit gallbladder were determined by using conventional (Kcl-filled) microelectrodes and Cl-selective, liquid ion-exchanger, microelectrodes. The results indicated that in the presence of a normal Ringer's solution, (Cl)c averages 35mM; this value is 2.3 times that predicted for an equilibrium distribution across the mucosal and baso-lateral membranes. On the other hand, when the tissue is bathed by Na-free solutions, (Cl)c declines to a value that does not differ significantly from that predicted for an equilibrium distribution. These results, together with those of Frizzell et al. (J. Gen. Physiol. 65:769, 1975) provide, for the first time, compelling evidence that (i) the movement of Cl from the mucosal solution into the cell is directed against an electrochemical potential difference (23mV); and (ii) this movement is energized by coupling to the entry of Na down a steep electrochemical potential difference. Finally, our data suggest that (i) Cl exit from the cell across the basolateral membrane may be coupled to the co-transport of a cation or the countertransport of an anion; and (ii) the mechanism responsible for active Na extrusion from the cell across the baso-lateral membrane is rheogenic (electrogenic), and is not the result of a neutral Na-K exchange.

Animals↗
PubMed1978

Ion transport by rabbit colon: II. Unidirectional sodium influx and the effects of amphotericin B and amiloride.

The unidirectional influx of Na from the mucosal solution into the epithelium of in vitro descending rabbit colon (JName) determined under short-circuit conditions, is comprised of two components: one represents entry of Na into transporting epithelial cells and is abolished by amiloride which also abolishes Na absorption (JNanet). The other represents diffusional Na entry into paracellular pathways traversing the epithelium. In all instances, exposure of the mucosal surface to amphotericin B increased tissue conductance and JName and elicited K secretion. Tissues showing a spontaneous Isc of approximately 4 microneq/cm2hr did not respond to amphotericin B with increased Isc and JNanet. However, in tissues characterized by a lower Isc under control conditions, amphotericin B increased Isc and JNanet to approximately 4 microneq/cm2 hr. These findings suggest that amphotericin increases JNanet and elicits K secretion by disrupting the normal perm-selectivity of the mucosal membrane. Under these conditions the extrusion of Na from cell-to-serosal solution becomes the rate limiting step in transepithelial Na transport. Finally, a close correlation between JName and JNanet was was observed when the rate of Na absorption varied either spontaneously or experimentally with amiloride, suggesting that the backflux of Na from cell-to-mucosal solution is undetectably small.

Amiloride↗
PubMed1978

Interaction between cell sodium and the amiloride-sensitive sodium entry step in rabbit colon.

Ouabain abolishes the short-circuit current (Isc) and decreases the transepithelial conductance (Gt) of rabbit colon. In contrast, amphotericin B elicits a maximum Isc and markedly increases Gt. However, in both instances the amiloride-sensitive Na entry step is completely blocked, presumably due to an increase in cell Na. Conversely, when Na-depleted tissues are suddenly exposed to 140 mM Na, the amiloride-sensitive Isc and the amiloride-sensitive component of Gt (alphaGNa) increase abruptly to their maximum values and then decline to steady-state plateaus with a half time of approximately 6 min; throughout the decline (Isc/alphaGNa) = ENa is constant at a value of 95 mV. In the presence of amphotericin B, the Isc abruptly rises to the same maximum but does not decline. These findings indicate that in the presence of 140 mM Na the conductance of the amiloride-sensitive Na entry step can vary from a maximum value of approximately 1.6 mmhos/cm2 when cell Na is depleted, to zero when cell Na is abnormally elevated (e.g., in the presence of ouabain or amphotericin B). Our findings are consistent with a system in which the pathway responsible for transcellular Na transport parallels another cellular compartment with which it communicates. The Na capacity of the active transport pathway appears to be very small so that this compartment fills rapidly after exposure of Na-depleted cells to 140 mM Na, and active transepithelial Na transport is initiated and reaches steady-state levels quickly. The Na capacity of the second compartment is much larger; the Na content of this compartment appears to be responsible for the negative feedback effect on the permeability of the amiloride-sensitive entry step.

Amiloride↗
PubMed1978

P-chloromercuribenzene sulfonate blocks and reverses the effect of amiloride on sodium transport across rabbit colon in vitro.

The addition of 10(-3) M p-chloromercuribenzene sulfonate (PCMBS) to the solution bathing the mucosal surface of rabbit colon has no effect on the rate of active Na transport but blocks or reverses the inhibitory action of amiloride. The tissue must be exposed to PCMBS for 20-30 min for a complete blocking effect, and removal of PCMBS from the mucosal solution after this period of exposure does not restore the sensitivity of the tissue to amiloride. The slow time-courses of the blocking and reversal effects suggest that PCMBS does not irreversibly interact with groups directly involved in the binding of amiloride.

4-Chloromercuribenzenesulfonate↗
PubMed1978

Influence of hexobendine, dipyridamole, dilazep, lidoflazine, inosine and purine riboside on adenosine uptake by the isolated epithelium of guinea pig jejunum.

The uptake of (14C)adenosine by isolated epithelium of guinea pig jejunum, administered on the blood side, was inhibited by hexobendine, dipyridamole, dilazep and lidoflazine. On the lumen side, however, weak inhibition was observed with lidoflazine only and no significant change was recorded with hexobendine, dipyridamole or dilazep. This difference was not altered when the degradation of hexobendine by the jejunal epithelium was blocked by physostigmine. When adenosine uptake was already reduced by purine riboside, further addition of hexobendine, dipyridamole, dilazep or lidoflazine caused divergent changes depending on the side of administration. Adenosine uptake was further diminished on the blood side, but raised towards control values on the lumen side. By contrast, inosine inhibited adenosine uptake on both sides of the epithleium. The results suggest that the mechanism of adenosine uptake is different on either side with respect to inhibition characteristics, corresponding to differences in morphology and function of the two sides of the intestinal epithelium.

Adenosine↗
PubMed1977

Effects of anions on amiloride-sensitive, active sodium transport across rabbit colon, in vitro. Evidence for "trans-inhibition" of the Na entry mechanism.

Replacement of Cl in the solutions bathing partial mucosal strips of rabbit descending colon with sulfate, isethionate, hydroxypropane-sulfonate and, to a lesser degree, ethanesulfonate stimulates active Na absorption (JNanet) when the baso-lateral pump mechanism is not saturated. These effects are rapid in onset and are readily reversible. Our findings indicate that these stimulatory anions decrease the resistance of the amiloridesensitive Na entry step at the mucosal membrane (RmNa). However, when the active Na pump mechanism at the baso-lateral membrane is saturated these stimulatory anions do not decrease the resistance of the Na entry process. These findings suggest the presence of a negative feedback between the activity of the pump mechanism and the resistance of the Na entry step which may be mediated by the size of the intracellular Na transport pool. In other words, it seems that when the baso-lateral pump is operating at its maximal rate the resistance to Na entry across the mucosal membrane through the amiloride-sensitive pathway is at a minimum and cannot be further decreased.

Amiloride↗
PubMed1977

Relaxation of coronary artery strips by adenosine and acidosis.

Cumulative dose-response curves of Ca2+-induced tension increments were studied in K+-depolarized helical strips of dog coronary arteries. Adenosine 10(-4) M reduced the Ca2+ sensitivity of the strips without altering the maximal tension with full Ca2+ activation. In contrast, acidosis of pH 7.05 significantly diminished the maximal tension with full Ca2+ activation. The relaxing effect of acidosis was almost completely abolished by 10(-4) M adenosine. It is concluded that adenosine inhibits Ca2+ influx, whereas acidosis depresses the contractile process of vascular smooth muscle directly.

Acidosis↗