Dihydroxy bile salt-induced secretion of rubidium ion across the rabbit distal colon

1987 ◽  
Vol 252 (4) ◽  
pp. G554-G561 ◽  
Author(s):  
R. W. Freel
Keyword(s):  
Bile Salt ◽  
Short Circuit ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Distal Colon ◽  
Simultaneous Measurements ◽  
K Secretion ◽  
Unidirectional Fluxes ◽  
Highly Correlated ◽  
K Transport

Possible mechanisms of dihydroxy bile salt-induced K+ secretion by the mammalian colon were evaluated by studying the effects of taurochenodeoxycholate (TCDC) on 86Rb+ transport across the isolated, short-circuited rabbit distal colon. Simultaneous measurements of 86Rb+ and 42K+ unidirectional fluxes were highly correlated [r = 0.964 for serosal (s) to mucosal (m) and 0.765 for m to s], indicating that Rb+ is a suitable tracer for K+ transport across the colon. Furthermore, mucosal Ba2+ (4 mM) or serosal ouabain (0.1 mM) decreased serosal to mucosal rubidium flux (JRbs----m) (from 0.24 +/- 0.02 to 0.09 +/- 0.02, and 0.08 +/- 0.01 mu eq X h-1 X cm-2, respectively) without affecting JRbm----s. Dibutyryl cyclic adenosine monophosphate (dBcAMP, 0.5 mM serosal) specifically increased JRbs----m of controls (from 0.21 +/- 0.05 to 0.67 +/- 0.09 mu eq X h-1 X cm-2) through a barium- (4 mM, mucosal) sensitive pathway without affecting JRbs----m. Mucosal addition of 2 mM TCDC increased tissue conductance (GT), reduced short-circuit (Isc) slightly, and reversed JRbnet (from 0.13 +/- 0.05 to -0.29 +/- 0.08 mu eq X h-1 X cm-2) principally by increasing JRbs----m. The TCDC-induced increases in JRbs----m were reduced by 0.1 mM serosal ouabain (from 0.53 +/- 0.03 to 0.11 +/- 0.02 mu eq X h-1 X cm-2) or 4 mM mucosal Ba2+ (from 0.76 +/- 0.07 to 0.32 +/- 0.04 mu eq X h-1 X cm-2).(ABSTRACT TRUNCATED AT 250 WORDS)

Active K transport across rabbit distal colon: relation to Na absorption and Cl secretion

1986 ◽  
Vol 251 (2) ◽  
pp. C252-C267 ◽  
Author(s):  
D. R. Halm ◽  
R. A. Frizzell
Keyword(s):  
Apical Membrane ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Secretory Process ◽  
Cl Secretion ◽  
K Secretion ◽  
Transport Inhibitors ◽  
Unidirectional Fluxes ◽  
K Transport

We measured isotopic unidirectional fluxes of K to elucidate the mechanisms of active K transport across the distal colon of the rabbit. Separate pathways for active K absorption and active K secretion were detected using various transport inhibitors and stimulators. The rate and direction of net K transport depend on the activities of these two pathways. K absorption was reduced by orthovanadate (both solutions) or serosal Ba, consistent with ATPase-dependent uptake of K across the apical membrane and exit via a Ba-sensitive basolateral K conductance. K secretion was inhibited by serosal ouabain or mucosal Ba, indicating that K secretion involves basolateral uptake via the Na-K pump and apical exit via a Ba-sensitive K conductance. Active K secretion appears to be electrogenic, since inhibition by ouabain produced equivalent changes in the net K flux and short-circuit current. Addition of bumetanide to the serosal solution or the removal of either Na or Cl from the serosal solution inhibited K secretion; mucosal solution amiloride was without effect. These results indicate that this K secretory process is independent of electrogenic Na absorption but is mechanistically similar to Cl secretory processes. Both epinephrine and prostaglandin E2 (PGE2) stimulate K secretion, but only PGE2 also stimulates Cl secretion. The response to these secretogogues suggests that the mechanisms underlying K and Cl secretion are closely linked but can be regulated independently.

K+ transport by rat colon: adaptation to a low potassium diet

1986 ◽  
Vol 250 (3) ◽  
pp. F483-F487
Author(s):  
R. L. Tannen ◽  
R. Marino ◽  
D. C. Dawson
Keyword(s):  
Rat Kidney ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Rat Colon ◽  
High K ◽  
Isotope Technique ◽  
K Secretion ◽  
Low K ◽  
K Transport

Recent studies with the isolated perfused rat kidney have demonstrated the existence of an intrinsic renal adaptation to conserve K+ in response to ingestion of a low K+ diet for 3 days. To determine whether the colon alters its K+ transport properties in a similar fashion, we measured transmural 86Rb fluxes across sheets of distal colonic epithelium under short-circuit conditions. Preliminary studies using a double-isotope technique demonstrated that 86Rb and 42K fluxes were similar; therefore 86Rb flux was considered equivalent to K+ flux. The distal half of the colon from each rat was divided into two segments, referred to as early and late distal colon. Experiments were carried out using rats fed a K+ -free, control (0.15 mmol/g), and high K+ (1.13 mmol/g) powdered diet of otherwise identical electrolyte content. Net K+ secretion (Jnet) by the early distal colon was reduced from 0.45 in the controls to -0.02 mueq X cm-2 X h-1 by a low K+ diet as a result of a decrease in serosal-to-mucosal flux (Jsm), with no change in mucosal-to-serosal flux (Jms). Conductance (GT) and short-circuit current (Isc) were unchanged. Jnet by the late distal colon averaged 0.17 in the controls and 0.01 mueq X cm-2 X h-1 with a low K+ diet, but this difference was not significant statistically. In comparison with the controls, a high K+ diet had no effect on Jnet by the early distal colon (0.48 mueq X cm-2 X h-1) but increased Jnet by the late distal colon substantially (0.77 mueq X cm-2 X h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

The Source of Short-Circuit Current Across Locust Rectum

1978 ◽  
Vol 77 (1) ◽  
pp. 107-122 ◽  
Author(s):  
D. WILLIAMS ◽  
J. E. PHILLIPS ◽  
W. T. PRINCE ◽  
J. MEREDITH
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Transport Processes ◽  
Rapid Decline ◽  
Tissue Viability ◽  
Bathing Medium ◽  
Flux Measurements ◽  
Unidirectional Fluxes ◽  
K Transport ◽  
Epithelial Resistance

Recta of desert locusts were mounted as flat sheets in ‘Ussing-type’ chambers and various parameters of tissue viability were monitored. The trans-epithelial resistance, the electropotential difference, the short-circuit current (Isc), and unidirectional fluxes of 22Na+, 36C1− and 42K+ all remained relatively constant during the 3rd and 4th h. The direction of the Isc indicated a net transport of either anions to the haemocoel, or cations to the lumen side. This current was abolished by KCN and was sensitive to temperature (Q10 = 2.4). There was a rapid decline in Isc over the first 2 h, which could be abolished by substituting NO3− or SO42- for Cl− in the bathing medium, indicating that this fall in current is due to a decline in the rate of Cl− transport. Measurements of 36C1− fluxes under short-circuit conditions confirm this interpretation. In the steady-state (3rd and 4th h), however, the same anion substitutions had no effect on IsC. Concurrent flux measurements indicated that net Na+ and K+ transport to the haemocoel side equals or slightly exceeds that of C1− in the same direction. Consequently all of the Isc must be due to unidentified ion transport processes. Transport of H+ to the lumen, or HCO3− and organic anions to the haemocoel side, is proposed.

Ion Transport Across the Midgut of the Tobacco Hornworm (Manduca Sexta)

1990 ◽  
Vol 150 (1) ◽  
pp. 425-442 ◽  
Author(s):  
M. E. CHAMBERLIN
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Tobacco Hornworm ◽  
Open Circuit ◽  
Middle Section ◽  
Anterior Section ◽  
K Secretion ◽  
K Transport ◽  
Subsequent Addition

1. The transport of K+, Na+ and Cl− across the three morphologically distinct regions of the tobacco hornworm midgut was measured under open-circuit and short-circuit conditions. Using a saline which contained physiological levels of haemolymph ions, amino acids and sugars, it was shown that all three sections actively secrete K+ and Cl− and absorb Na+. 2. The anterior section maintained the highest short-circuit current (Isc), transepithelial potential difference (PD) and net K+ secretion. The middle section had the lowest Isc, PD and K+ secretion, but absorbed Na+ at the greatest rate. The posterior section had the greatest rate of Cl− secretion. 3. Omission of K+ depressed the Isc. Subsequent addition of K+ stimulated the Isc to control levels in the middle and posterior sections, but not in the anterior section. Omission of Cl− or Na+ also inhibited the Isc. Reintroduction of Cl− had no stimulatory effect and, although reintroduction of Na+ stimulated the Isc, control levels were not attained. 4. Unlike the results reported in previous studies, the net K+ transport exceeded the Isc in all three midgut sections. The deficit in Isc was not made up by the transport of Na+ and Cl−. The results are discussed with respect to proposed models of ion transport across this epithelium.

Amphotericin B and K+ transport across excised toad urinary bladder

1979 ◽  
Vol 237 (2) ◽  
pp. F145-F156
Author(s):  
J. T. Gatzy ◽  
L. Reuss ◽  
A. L. Finn
Keyword(s):  
Isotope Exchange ◽  
Fold Increase ◽  
Toad Urinary Bladder ◽  
Bathing Solution ◽  
Na Transport ◽  
Drug Induced ◽  
K Secretion ◽  
Unidirectional Fluxes ◽  
Induced Changes ◽  
K Transport

The transmural electric PD of bladders bathed by Na2SO4 Ringer was not affected by amphotericin (5 x 10(-6) M, mucosal) but the PD followed the direction for K+ diffusion in the presence of a transmural K+ gradient. Increases in bathing solution K+ increased conductance. Ouabain pretreatment did not affect drug-induced changes in PD or conductance. Unidirectional fluxes of radiolabeled Na+ and K+ but not SO42- across the short-circuited bladder were increased by amphotericin. Ninety percent of the rise in the serosal-to-mucosal flow of Na+ disappeared when mucosal Na+ was replaced by choline. Amphotericin induced a 20-fold increase in mucosal-to-serosal K+ flux but K+ serosal-to-mucosal flow increased 200-fold. This flux asymmetry persisted for 110 min, was abolished by pre- or posttreatment with ouabain, and was immeasurable when bathing solution K+ was increased from 2.4 to 59 meq/liter. With 2.4 meq K+/liter the ratio of active Na+ reabsorption to K+ secretion was 8 to 1, but K+ secretion was not closely linked to Na+ transport. The results suggest that amphotericin induces a paracellular K+-selective path, Na+ isotope exchange, and K+ secretion.

Aldosterone stimulates K secretion prior to onset of Na absorption in guinea pig distal colon

1994 ◽  
Vol 266 (2) ◽  
pp. C552-C558 ◽  
Author(s):  
D. R. Halm ◽  
S. T. Halm
Keyword(s):  
Guinea Pig ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Ussing Chambers ◽  
High Affinity Receptor ◽  
Additive Increase ◽  
K Secretion ◽  
Affinity Receptor

Distal colon from guinea pig was stimulated in vitro by aldosterone in Ussing chambers that allowed measurement of short-circuit current (Isc) and tissue conductance (Gt). The response to aldosterone was delayed by approximately 20 min and resulted in a negative Isc, consistent with K secretion. Approximately 1 h later the Isc began to increase and eventually became positive, consistent with subsequent stimulation of Na absorption. The Na-absorptive response could be inhibited by mucosal amiloride without altering the rate of K secretion. Similarly, K secretion could be inhibited by serosal bumetanide without altering Na absorption. In the presence of spironolactone, actinomycin D, or cycloheximide, aldosterone failed to stimulate both K secretion and Na absorption. A dose response to aldosterone provided an apparent Kd of 2.6 +/- 0.5 nM, consistent with a high-affinity receptor coupled to this secretory response. Stimulation by the K secretagogue epinephrine did not produce an additive increase in K secretion, suggesting that the same cell type responds to both aldosterone and epinephrine and that the protein induced by aldosterone was not one of the membrane proteins responsible for K secretion.

scholarly journals Role of the BK channel (KCa1.1) during activation of electrogenic K+ secretion in guinea pig distal colon

2012 ◽  
Vol 303 (12) ◽  
pp. G1322-G1334 ◽  
Author(s):  
Jin Zhang ◽  
Susan T. Halm ◽  
Dan R. Halm
Keyword(s):  
Guinea Pig ◽  
Apical Membrane ◽  
Splice Variants ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Bk Channel ◽  
Prostaglandin E ◽  
Maximal Inhibition ◽  
K Secretion

Secretagogues acting at a variety of receptor types activate electrogenic K+ secretion in guinea pig distal colon, often accompanied by Cl− secretion. Distinct blockers of KCa1.1 (BK, Kcnma1), iberiotoxin (IbTx), and paxilline inhibited the negative short-circuit current ( Isc) associated with K+ secretion. Mucosal addition of IbTx inhibited epinephrine-activated Isc (epi Isc) and transepithelial conductance (epi Gt) consistent with K+ secretion occurring via apical membrane KCa1.1. The concentration dependence of IbTx inhibition of epi Isc yielded an IC50 of 193 nM, with a maximal inhibition of 51%. Similarly, IbTx inhibited epi Gt with an IC50 of 220 nM and maximal inhibition of 48%. Mucosally added paxilline (10 μM) inhibited epi Isc and epi Gt by ∼50%. IbTx and paxilline also inhibited Isc activated by mucosal ATP, supporting apical KCa1.1 as a requirement for this K+ secretagogue. Responses to IbTx and paxilline indicated that a component of K+ secretion occurred during activation of Cl− secretion by prostaglandin-E2 and cholinergic stimulation. Analysis of KCa1.1α mRNA expression in distal colonic epithelial cells indicated the presence of the ZERO splice variant and three splice variants for the COOH terminus. The presence of the regulatory β-subunits KCaβ1 and KCaβ4 also was demonstrated. Immunolocalization supported the presence of KCa1.1α in apical and basolateral membranes of surface and crypt cells. Together these results support a cellular mechanism for electrogenic K+ secretion involving apical membrane KCa1.1 during activation by several secretagogue types, but the observed K+ secretion likely required the activity of additional K+ channel types in the apical membrane.

cGMP and Ca2+ regulation of ion transport across the isolated porcine distal colon epithelium

1994 ◽  
Vol 267 (4) ◽  
pp. R1026-R1033 ◽  
Author(s):  
M. D. DuVall ◽  
S. M. O'Grady
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Ussing Chambers ◽  
Cl Secretion ◽  
Nacl Absorption ◽  
Flux Measurements ◽  
K Secretion ◽  
Baseline Values ◽  
Distal Colon Epithelium

Intact epithelium from the porcine distal colon was stripped of serosal muscle and mounted in Ussing chambers to investigate the regulation of Na, Cl, and K transport by guanosine 3',5'-cyclic monophosphate (cGMP) and elevations in intracellular [Ca2+]. Under voltage-clamped conditions cGMP (250 microM) produced an increase in tissue short-circuit current (Isc) that reached a maximal value within 10-20 min and remained elevated > 40 min. This response was associated with an inhibition of NaCl absorption and stimulation of Cl and K secretion. In the absence of Cl the Isc also slowly increased but returned to baseline values within 20 min. Bicarbonate removal from both serosal and mucosal solutions or serosal bumetanide (20 microM) reduced the effect of cGMP on Isc by approximately 40%. When performed simultaneously, these conditions reduced the cGMP response by approximately 60%. Transepithelial Na and Cl flux measurements indicated that serosal bumetanide blocked increased Cl secretion without effecting changes in NaCl absorption. In contrast, mucosal amiloride blocked the effects of cGMP on NaCl absorption but not Cl secretion. The cGMP Isc response was potentiated in the presence of 1 mM, but not 10 microM, amiloride. Moreover, 1 mM amiloride inhibited Isc under control conditions but was ineffective in the presence of cGMP. The Ca2+ ionophore ionomycin (3 microM) produced a transient increase in the Isc that was also associated with a decrease in transepithelial NaCl absorption and an increase in Cl and K secretion. In contrast to cGMP, the ionomycin Isc response was eliminated after Cl removal from the bath.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Cyclic AMP-induced K+secretion occurs independently of Cl−secretion in rat distal colon

2012 ◽  
Vol 303 (3) ◽  
pp. C328-C333 ◽  
Author(s):  
Geoffrey I. Sandle ◽  
Vazhaikkurichi M. Rajendran
Keyword(s):  
Channel Blocker ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Secretory Diarrhea ◽  
Atpase Inhibitor ◽  
Rat Distal Colon ◽  
Electrogenic Ion Transport ◽  
K Secretion

cAMP induces both active Cl−and active K+secretion in mammalian colon. It is generally assumed that a mechanism for K+exit is essential to maintain cells in the hyperpolarized state, thus favoring a sustained Cl−secretion. Both Kcnn4c and Kcnma1 channels are located in colon, and this study addressed the questions of whether Kcnn4c and/or Kcnma1 channels mediate cAMP-induced K+secretion and whether cAMP-induced K+secretion provides the driving force for Cl−secretion. Forskolin (FSK)-enhanced short-circuit current (indicator of net electrogenic ion transport) and K+fluxes were measured simultaneously in colonic mucosa under voltage-clamp conditions. Mucosal Na+orthovanadate (P-type ATPase inhibitor) inhibited active K+absorption normally present in rat distal colon. In the presence of mucosal Na+orthovanadate, serosal FSK induced both K+and Cl−secretion. FSK-induced K+secretion was 1) not inhibited by either mucosal or serosal 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34; a Kcnn4 channel blocker), 2) inhibited (92%) by mucosal iberiotoxin (Kcnma1 channel blocker), and 3) not affected by mucosal cystic fibrosis transmembrane conductance regulator inhibitor (CFTRinh-172). By contrast, FSK-induced Cl−secretion was 1) completely inhibited by serosal TRAM-34, 2) not inhibited by either mucosal or serosal iberiotoxin, and 3) completely inhibited by mucosal CFTRinh-172. These results indicate that cAMP-induced colonic K+secretion is mediated via Kcnma1 channels located in the apical membrane and most likely contributes to stool K+losses in secretory diarrhea. On the other hand, cAMP-induced colonic Cl−secretion requires the activity of Kcnn4b channels located in the basolateral membrane and is not dependent on the concurrent activation of apical Kcnma1 channels.

EFFECT OF IODIDE ON THE ADENYL CYCLASE SYSTEM OF THE MOUSE THYROID IN VIVO

1978 ◽  
Vol 88 (3) ◽  
pp. 517-527 ◽  
Author(s):  
C. Saddok ◽  
M. Gafni ◽  
J. Gross
Keyword(s):  
Cyclic Adenosine Monophosphate ◽  
Iodine Content ◽  
Adenosine Monophosphate ◽  
Iodine Intake ◽  
Adenyl Cyclase ◽  
Camp Accumulation ◽  
Adenyl Cyclase Activity ◽  
Pre Treatment ◽  
Highly Correlated

ABSTRACT Iodide, administered to mice either acutely or chronically, depressed the thyroidal cyclic adenosine monophosphate (cAMP) response to 20 mU bovine TSH. When iodide was administered acutely there was a 60% reduction in the cAMP accumulation after 100 μg, or 1 μg KI given to mice on normal iodine diet (NID), or low iodine diet (LID), respectively. When iodide was administered chronically by supplementing the LID with graded doses of KI for 11 days, the cAMP response to TSH was found to be inversely related to the dietary iodine. Inhibition occurred after 5 μg KI, a dose similar to the daily iodine intake. Iodide depressed, but did not abolish, the thyroidal cAMP response to TSH. Iodide had no effect on phosphodiesterase activity, whereas thyroidal adenyl cyclase activity was diminished by the prior administration of 100 μg KI. The iodide effect was abolished by pre-treatment with methylmercaptoimidazole i.e. the inhibition is related to iodide oxidation. The newly organified thyroidal iodine (NOTI), formed at 2 h from 0.1–1000 μg KI was determined. The amount of NOTI was highly correlated to the degree of inhibition, irrespective of the iodine content of the diet. This relationship was continuous up to 100 ng NOTI and 70% inhibition, which are the maximal values obtained for NOTI formation and inhibition of cAMP accumulation. These plateau levels were reached with 100 or 1 μg KI in mice on NID or LID, respectively. These results indicate that the inhibitor is an iodinated substance whose intrathyroidal formation is quantitatively parallel to, or a part of NOTI.

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