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R Greger

Publications and source records attributed to R Greger.

At least 55 records · Page 3Linked to original sources
PubMed1989

Macula densa cells sense luminal NaCl concentration via furosemide sensitive Na+2Cl-K+ cotransport.

The macula densa cells of the juxtaglomerular apparatus probably serve as the sensor cells for the signal which leads to the appropriate tubuloglomerular feedback response. The present study reports basolateral membrane voltage (PDbl) measurements in macula densa cells. We isolated and perfused in vitro thick ascending limb segments with the glomerulus, and therefore the macula densa cells, and the early distal tubule still attached. Macula densa cells were impaled with microelectrodes under visual control. PDbl was recorded in order to examine how these cells sense changes in luminal NaCl concentrations. The addition of furosemide, a specific inhibitor of the Na+2Cl-K+ cotransporter in the thick ascending limb, to the lumen of the perfused thick ascending limb hyperpolarized PDbl from -55 +/- 5 mV to -79 +/- 4 mV (n = 7). Reduction of NaCl in the lumen perfusate from 150 mmol/l to 30 mmol/l also hyperpolarized PDbl from -48 +/- 3 mV to -66 +/- 5 mV (n = 4). A Cl- concentration step in the bath from 150 mmol/l to 30 mmol/l resulted in a 24 +/- 4 mV (n = 4) depolarization of PDbl. This depolarization of PDbl was absent when furosemide was present during the Cl- concentration step. These data suggest that the macula densa cells sense changes in luminal NaCl concentration via coupled uptake of Na+ and Cl-.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Characterization of potassium channels in respiratory cells. I. General properties.

Potassium channels present in the basolateral membrane of respiratory epithelial cells play an important role in the process of chloride secretion. Utilizing the patch clamp technique, we examined human cultured respiratory epithelial cells derived from patients with cystic fibrosis (CF) and normals individual (N) for the existence of and for the properties of K+ channels. We obtained qualitatively and quantitatively identical results for both preparations (CF and N). K+ channels were spontaneously present in cell attached patches. The channels showed burst appearance with rapid flickering within the bursts. When the pipette was filled with 145 mmol/l KCl, a mean conductance of 131 +/- 25 pS (n = 15) was read from the I/V-curve at a clamp voltage (Vc) of 0 mV. After excision, the conductance read from the I/V-curve at Vc = 0 mV was 212 +/- 11 pS (Pipette: 145 mmol/l KCl, bath: 145 mmol/l NaCl) (n = 61). With NaCl in the pipette and KCl in the bath, a similar conductance was obtained (g = 210 pS; n = 2). When both, pipette and bath contained KCl, the conductance was increased to 302 +/- 19 (n = 7). The channel was highly selective for potassium over sodium: PK + /PNa + greater than 40. The channel open probability was only slightly voltage dependent i.e. the open probability increased slightly with depolarisation. For most of the channels one open time constant (to = 6.3 +/- 1.6 ms; n = 22) and one closed time constant (tc = 1.8 +/- 0.3 ms; n = 21) was obtained.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Membrane↗
PubMed1989

Characterization of potassium channels in respiratory cells. II. Inhibitors and regulation.

In a previous study [26] we described the properties of potassium channels in cultured respiratory cells derived from cystic fibrosis patients (CF) and normal individuals (N). In the present study we examine the regulatory mechanisms of these channels by the patch clamp technique. Since there were no apparent differences in the properties of CF and N K+ channels the results were pooled. In the excised inside/out configuration the channel was blocked by different K+ channel blockers. Barium (5.10(-3) mol/l), tetraethylammoniumchloride (5.10(-3) mol/l), quinidine (10(-3) mol/l) and lidocaine (5.10(-3) mol/l), when added to the cytosolic side, inhibited K+ channels reversibly. An increase in the calcium concentration from 10(-7) mol/l to 10(-6) mol/l led to a marked increase in the open channel probability (Po). Further increases in Ca2+ concentration increased Po only slightly. No pH effects on the cytosolic side of the channel were observed. The channel open probability was reduced when ATP was present on the cytosolic side at a concentration of 10(-4) mol/l to 10(-3) mol/l. Non hydrolysable adenosine 5'-[beta, gamma-methylene] triphosphate had the same inhibitory effect as ATP. The inhibition by ATP was blunted by the simultaneous addition of 1 mmol/l ADP. The inhibition of K+ channels by cytosolic ATP may represent a channel regulatory mechanism in the intact cell. This would allow for coupling between the activity of the (Na+ + K+)-pump and the basolateral K+ conductance.

Adenosine Triphosphate↗
PubMed1989

Piretanide-dextran and piretanide-polyethylene glycol interact with high affinity with the Na+ 2 Cl- K+ cotransporter in the thick ascending limb of the loop of Henle.

Piretanide blocks the Na+ 2Cl- K+ cotransporter protein in the thick ascending limb (TAL) of the loop of Henle reversibly. When tested from the luminal side in isolated perfused cTAL segments it leads to a half maximal inhibition (IC50) of the equivalent short circuit current (Isc) at a concentration of 10(-6) mol/l. From the basolateral side it has no effect on Isc up to 10(-4) mol/l. The present study was designed to search for high affinity blockers of the Na+ 2Cl- K+ cotransporter with large molecular weight in an attempt to use these macromolecules for antibody-labelling or affinity separation of this transport-protein. Amino-ethyl-dextran or amino-ethyl-polyethylene glycol (M.W. 5kd) were coupled to isothiocyanato-piretanide (ISO-PIR) at room temperature in DMSO. The resulting compounds dextran-sulfonylurea-piretanide (PIR-DEX) and polyethylene glycol-sulfonylurea-piretanide (PIR-PEG) (M.W. 5.38kd) were purified and tested in isolated perfused cTAL segments. IC50 values for ISO-PIR, PIR-DEX and PIR-PEG were estimated from dose response curves after their addition to the lumen or bath perfusate, respectively. ISO-PIR, PIR-DEX and PIR-PEG acted from the lumen side at 3.10(-6), 6.10(-6) and 2.10(-6) mol/l. The inhibitory effect was easily reversible. From the basolateral side no effect for any compound was seen at up to 10(-4) mol/l. In clearance experiments PIR-DEX was given to female Wistar rats as an i.v. bolus (25 mumol/kg) and the diuretic urine was collected. After dialysis (exclusion limit 2.5kd) the dialysed urine and the dialysate were tested in isolated perfused cTAL segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Blocking kinetics of Cl- channels in colonic carcinoma cells (HT29) as revealed by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB).

The blocking effect of 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) was investigated on single Cl- channels of the cultured human colon carcinoma cells, HT29. In the absence of NPPB, the open-time histogram yielded two time constants, with 0.9 ms and 33 ms, whereas the closed-time distribution could be fitted by a single exponential with a time constant of 0.7 ms. Addition of NPPB in the range 1-50 microM induced brief closing events of the single-channel current. This resulted in a decrease of the long open-time constant to 2.1 ms and in an increase of the closed-time constant to 1.8 ms at 50 microM NPPB concentration. The short open-time constant did not change at low blocker concentration (1 microM), but could no longer be resolved at higher concentrations. The open-state probability decreased from 0.9 (control conditions) to 0.5 at 50 microM NPPB. The Hill plot yielded a Hill coefficient of about 0.7, compatible with one NPPB molecule inhibiting one channel molecule. The kinetics of channel gating are described by a sequential model with one closed and two open states. Since in the presence of NPPB no additional time constant appeared in the time histograms, we assumed the same kinetic scheme as under control conditions, and hypothesize that NPPB has an influence on rate constants.

Cell Line↗
PubMed1988

Electrophysiological study of transport systems in isolated perfused pancreatic ducts: properties of the basolateral membrane.

In order to study the mechanism of pancreatic HCO3- transport, a perfused preparation of isolated intra- and interlobular ducts (i.d. 20-40 microns) of rat pancreas was developed. Responses of the epithelium to changes in the bath ionic concentration and to addition of transport inhibitors was monitored by electrophysiological techniques. In this report some properties of the basolateral membrane of pancreatic duct cells are described. The transepithelial potential difference (PDte) in ducts bathed in HCO3(-)-free and HCO3(-)-containing solution was -0.8 and -2.6 mV, respectively. The equivalent short circuit current (Isc) under similar conditions was 26 and 50 microA . cm-2. The specific transepithelial resistance (Rte) was 88 omega cm2. In control solutions the PD across the basolateral membrane (PDbl) was -63 +/- 1 mV (n = 314). Ouabain (3 mmol/l) depolarized PDbl by 4.8 +/- 1.1 mV (n = 6) within less than 10 s. When the bath K+ concentration was increased from 5 to 20 mmol/l, PDbl depolarized by 15.9 +/- 0.9 mV (n = 50). The same K+ concentration step had no effect on PDbl if the ducts were exposed to Ba2+, a K+ channel blocker. Application of Ba2+ (1 mmol/l) alone depolarized PDbl by 26.4 +/- 1.4 mV (n = 19), while another K+ channel blocker TEA+ (50 mmol/l) depolarized PDbl only by 7.7 +/- 2.0 mV (n = 9). Addition of amiloride (1 mmol/l) to the bath caused 3-4 mV depolarization of PDbl. Furosemide (0.1 mmol/l) and SITS (0.1 mmol/l) had no effect on PDbl. An increase in the bath HCO3- concentration from 0 to 25 mmol/l produced fast and sustained depolarization of PDbl by 8.5 +/- 1.0 mV (n = 149). It was investigated whether the effect of HCO3- was due to a Na+-dependent transport mechanism on the basolateral membrane, where the ion complex transferred into the cell would be positively charged, or whether it was due to decreased K+ conductance caused by lowered intracellular pH. Experiments showed that the HCO3- effect was present even when the bath Na+ concentration was reduced to a nominal value of 0 mmol/l. Similarly, the HCO3- effect remained unchanged after Ba2+ (5 mmol/l) was added to the bath. The results indicate that on the basolateral membrane of duct cells there is a ouabain sensitive (Na+ + K+)-ATPase, a Ba2+ sensitive K+ conductance and an amiloride sensitive Na+/H+ antiport. The HCO3- effect on PDbl is most likely due to rheogenic anion exit across the luminal membrane.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1988

Properties of the luminal membrane of isolated perfused rat pancreatic ducts. Effect of cyclic AMP and blockers of chloride transport.

The aim of the present study was to investigate by what transport mechanism does HCO-3 cross the luminal membrane of pancreatic duct cells, and how do the cells respond to stimulation with dibutyryl cyclic AMP (db-cAMP). For this purpose a newly developed preparation of isolated and perfused intra- and interlobular ducts of rat pancreas was used. Responses of the epithelium to inhibitors and agonists were monitored by electrophysiological techniques. Addition of HCO-3/CO2 to the bath side of nonstimulated ducts depolarized the PD across the basolateral membrane (PDbl) by about 9 mV, as also observed in a previous study [21]. This HCO-3 effect was abolished by Cl- channel blockers or SITS infused into the lumen of the duct: i.e. 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB, 10(-5) M) hyperpolarized PDbl by 8.2 +/- 1.6 mV (n = 13); 3',5-dichlorodiphenylamine-2-carboxylic acid (DCl-DPC, 10(-5) M) hyperpolarized PDbl by 10.3 +/- 1.7 mV (n = 10); and SITS hyperpolarized PDbl by 7.8 +/- 0.9 mV (n = 4). Stimulation of the ducts with db-cAMP in the presence of bath HCO-3/CO2 resulted in depolarization of PDbl, the ductal lumen became more negative and the fractional resistance of the luminal membrane decreased. Together with forskolin (10(-6) M), db-cAMP (10(-4) M) caused a fast depolarization of PDbl by 33.8 +/- 2.5 mV (n = 6). When db-cAMP (5 x 10(-4) M) was given alone in the presence of bath HCO-3/CO2, PDbl depolarized by 25.3 +/- 4.2 mV (n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1988

Differential effects of ADH on sodium, chloride, potassium, calcium and magnesium transport in cortical and medullary thick ascending limbs of mouse nephron.

The effect of antidiuretic hormone (arginine vasopressin, AVP) on transepithelial Na+, Cl-, K+, Ca2+ and Mg2+ net transports was investigated in medullary (mTAL) and cortical (cTAL) segments of the thick ascending limb (TAL) of mouse nephron, perfused in vitro. Transepithelial net fluxes (JNa+, JCl-, JK+, JCa2+, JMg2+) were determined by electron probe analysis of the collected tubular fluid. Transepithelial potential difference (PDte) and transepithelial resistance (Rte) were measured simultaneously. cTAL segments were bathed and perfused with isoosmolal, HCO3- containing Ringer solutions, mTAL segments were bathed and perfused with isoosmolal HCO3- free Ringer solutions. In cTAL segments, AVP (10(-10) mol.l-1) significantly increased JMg2+ and JCa2+ from 0.39 +/- 0.08 to 0.58 +/- 0.10 and from 0.86 +/- 0.13 to 1.19 +/- 0.15 pmol.min-1 mm-1 respectively. Neither JNa+ nor JCl-, (JNa+: 213 +/- 30 versus 221 +/- 28 pmol.min-1 mm-1, JCl-: 206 +/- 30 versus 220 +/- 23 pmol.min-1 mm-1) nor PDte (13.4 +/- 1.3 mV versus 14.1 +/- 1.9 mV) or Rte (24.6 +/- 6.5 omega cm2 versus 22.6 +/- 6.4 omega cm2) were significantly changed by AVP. No significant effect of AVP on net K+ transport was observed. In mTAL segments, Mg2+ and Ca2+ net transports were close to zero and AVP (10(-10) mol.l-1) elicited no effect. However NaCl net reabsorption was significantly stimulated by the hormone, JNa+ increased from 107 +/- 33 to 148 +/- 30 and JCl- from 121 +/- 33 to 165 +/- 32 pmol.min-1 mm-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Stimulation of NaCl secretion in the rectal gland of the dogfish Squalus acanthias.

1. The rectal gland of the dogfish (Squalus acanthias) secretes NaCl when stimulated by a hormone related to vasointestinal peptide. 2. Patch clamp and microelectrode techniques are used to examine the changes in membrane conductances occurring with hormonal stimulation. 3. The conductance of the "resting" cell is dominated by basolateral K+ channels. 4. Hormonal stimulation "opens" apical Cl- channels. 5. This opening of apical chloride channels appears to be mediated by cAMP-dependent phosphorylation of pre-existing closed channels.

Animals↗
PubMed1988

Inhibition of active NaCl reabsorption in the thick ascending limb of the loop of Henle by torasemide.

The new diuretic torasemide (1-isopropyl-3- ([4-(3-methyl-phenylamino)pyridine]-3-sulfonyl)urea) was tested in isolated in vitro perfused cortical thick ascending limbs of Henle loops of rabbit kidney. The equivalent short circuit current (Isc) corresponding in this nephron segment to the rate of secondarily active Cl-reabsorption was measured continuously. Torasemide led to a rapid and reversible inhibition of Isc when added to the luminal perfusate. The IC50 for this effect was 3 x 10(-7) mol/l. A similar effect was also exerted by torasemide addition to the peritubular bath. However, 100 times larger doses were needed. The data are compatible with the view that torasemide interacts with both, the Na+2Cl-K+ carrier, localized in the luminal membrane, and, at higher concentrations, with the chloride channels present in the basolateral membrane of this nephron segment. Under normal conditions, and in the intact kidney, the former effect, i.e. interference with the Na+2Cl-K+ carrier will be the dominant action of this drug.

Absorption↗
PubMed1987

Potassium conductance in straight proximal tubule cells of the mouse. Effect of barium, verapamil and quinidine.

The present study has been performed to test for the influence of verapamil and quinidine on the potential difference across the basolateral cell membrane (PDbl) and on the basolateral potassium conductance of isolated perfused segments of the mouse proximal tubule. PDbl was recorded continuously with conventional microelectrodes during rapid alterations of bath or luminal perfusate composition. The contribution of the basolateral potassium conductance to the conductance of both cell membranes (tk) was estimated from the effects of altered bath potassium concentration on PDbl. Under control conditions tk approaches 0.8, i.e. the basolateral cell membrane is mainly conductive to potassium. Neither quinidine nor verapamil affect PDbl at concentrations below 10 mumol/l. At higher concentrations both substances depolarize the basolateral cell membrane mimicking the effect of 1 mmol/l barium. In the presence of 0.1 mmol/l verapamil tk is virtually abolished at 5 to 10 mmol/l bath potassium concentration but is almost unaffected at bath potassium concentrations between 20 and 40 mmol/l. 1 mumol/l ionophore A-23187 does not change the depolarizing effect of 0.1 mmol/l verapamil on cell membrane potential. In the presence of 0.1 mmol/l quinidine, tk is reduced to some 50%, irrespective of the bath potassium concentration. It is concluded that the potassium conductance in straight proximal tubules is inhibited not only by barium but as well by high concentrations of verapamil and quinidine. The effect is probably direct and not related to alterations in the intracellular calcium activity.

Animals↗
PubMed1987

Properties of single K+ channels in the basolateral membrane of rabbit proximal straight tubules.

The basolateral membrane of rabbit straight proximal tubules, which were cannulated and perfused on one side, was investigated with the patch clamp technique. Properties of inward and outward directed single K+ channel currents were studied in cell-attached and inside-out oriented cell-excised membrane patches. In cell-attached patches with NaCl Ringer solution both in pipette and bath, outward K+ currents could be detected after depolarization of the membrane patch by about 20-30 mV. The current-voltage (i/V) relationship could be fitted by the Goldman-Hodgkin-Katz (GHK) current equation, with the assumption that these channels were mainly permeable for K+ ions. A permeability coefficient PK of (0.17 +/- 0.04).10(-12) cm3/s was obtained, the single channel slope conductance at infinite positive potential g(V infinity) was 50 +/- 12 pS and the single channel conductance at the membrane resting potential g(Vbl) was 12 +/- 3 pS (n = 4). In cell-excised patches, with NaCl in the pipette and KCl in the bath, the data could also be fitted to the GHK equation and yielded PK = (0.1 +/- 0.01).10(-12) cm3/s, g(V infinity) = 40 +/- 4 pS and g(Vbl) = 7 +/- 1 pS (n = 8). In cell-attached patches with KCl in the pipette and NaCl in the bath, inward K+ channels occurred at clamp potentials less than or equal to 60 mV, whereas outward K+ channel current was detected at more positive voltages. The current-voltage curves showed slight inward rectification.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The diuretic effect of muzolimine.

Muzolimine produces a diuresis in the loop of Henle. Unlike other diuretics of this kind, the effect of muzolimine is slow and its action is long lasting. The present study was designed to examine the mechanism of action of muzolimine in isolated in vitro perfused rabbit cortical thick ascending limb segments (cTAL). In a first series it was confirmed that muzolimine itself in a concentration of up to 10(-4) mol/l had no effect on the equivalent short circuit current (Isc), corresponding to the rate of active NaCl reabsorption, in cTAL segments neither from the lumen nor from the bath side. In a second series of experiments, muzolimine was administered intravenously (70 mumol/kg) to male Wistar rats, and the clearances of inulin, Na+ and K+ were calculated. Muzolimine, after a lag phase of 5 to 20 min caused a marked diuresis and natriuresis, but had only a minor effect on glomerular filtration rate and on K+ excretion. The urines of these animals were diluted with isotonic saline, and were examined in rabbit cTAL segments for their ability to block Isc. It was found that the urines of the antidiuretic period were devoid of effects, whereas the diuretic urines inhibited Isc strongly down to a dilution of 300 times when they were perfused in the lumen. The same diluted urines had no effect from the bath side. In a third series, probenecid (100 mumol/kg) was administered i.v. to rats undergoing a muzolimine induced saluresis. It was found that probenecid inhibited the diuresis and saluresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Analogues of torasemide--structure function relationships--experiments in the thick ascending limb of the loop of Henle of rabbit nephron.

The aim of the present study was to examine compounds related to torasemide with respect to their ability to block the equivalent short circuit current, corresponding to the rate of chloride reabsorption, in isolated in vitro perfused cortical thick ascending limbs of Henle of the rabbit. The torasemide molecule was modified with respect to the anionic sulfonylurea group, and the secondary amine linked to the pyridine ring. Our results indicate that only few of the tested 48 torasemide-related compounds were able to inhibit from both epithelial sides like torasemide. Only few of the tested compounds were equally effective as torasemide from the lumen side. Some analogues were acting only from the luminal side and some only from the peritubular side. The correlations between structure and potency of inhibition from the luminal side allow the following conclusions: The secondary amine moiety linked to the pyridine ring (toluidine in case of torasemide) can be replaced by a cycloalkylamine or, with some loss of inhibitory potency, by alkylamines. The inhibitory potency is increased with the number of C-atoms in the cycloalkylamine substituted compounds (optimum C7 to C8) and is also depending on the length of the alkylamines (optimum C4). The secondary amine seems to be required since nitrogen cannot be replaced by -S- or -SO2-. The sulfonylurea group cannot be substituted by other anionic groups such as -SO-3 or -COO-. If the pyridine ring is replaced by a NO2-substituted phenyl ring, the inhibitory potency from the luminal side is lost. However, these compounds act still (with some loss of potency) from the peritubular side.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Potassium channels in the basolateral membrane of the rectal gland of the dogfish (Squalus acanthias).

Previous studies in isolated, in vitro perfused rectal gland tubules (RGT) have revealed that the basolateral membrane possesses a K+ conductive pathway. In the present study, we have utilized the patch clamp technique in RGT segments to characterize this pathway. The basolateral membrane was approached with patch pipettes at the open end of in vitro perfused segments. Recordings were obtained in cell-attached as well as in excised inside-out patches. In cell-attached patches with the pipette filled with a KCl solution (274 mmol/l) and the bath containing NaCl shark Ringer (275 mmol/l), inward K+ currents (from pipette into cell) with a mean slope conductance of 123 +/- 26 pS (n = 3) were observed. We were unable to generate outward K+ currents at high depolarizing (cell more positive) clamp voltages. This indicates inward rectification of this channel. To examine the rectification properties further, excised (inside out) patches were exposed to K+ concentration gradients, directed out of, as well as into the pipette. With NaCl in the pipette and KCl in the bath, K+ outward currents were observed. The current-voltage (IV) relation revealed Goldman-type rectification, with a mean single channel conductance of 185 +/- 28 pS (n = 7) at high positive voltages (linear range of the IV curve). The single-channel permeability coefficient for K+ was 0.26 +/- 0.04 X 10(-12) cm3/s (n = 7). In the reversed experiment (pipette KCl, bath NaCl), inward currents of similar kinetics and amplitude were obtained. The single channel conductance was 146 +/- 21 pS (n = 7) at high negative voltages (linear range of the IV curve).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Potassium channels in the basolateral membrane of the rectal gland of Squalus acanthias. Regulation and inhibitors.

The present study examines the influences of pH and Ca2+ and several putative inhibitors on the basolateral K+ channel of the rectal gland of Squalus acanthias. Excised membrane patches were examined using the patch clamp technique. It is shown that reduction of the calcium activity on the cytosolic side to less than 10(-9) mol/l has no detectable inhibitory effect on this channel. Conversely, increase in calcium activity to some 10(-3) mol/l reduced the activity of this channel. Variations in cytosolic pH had only a moderate effect on the current amplitude: alkalosis by one pH unit increased and acidosis reduced the single current amplitude by some 15%. Several inhibitors were tested in excised patches when added to the cytosolic side. Ba2+ (approximately 5 X 10(-3) mol/l), quinine (approximately 10(-3) mol/l), quinidine (approximately 10(-4) mol/l), lidocaine (approximately equal to 1 mmol/l), tetraethylammonium (approximately 10 mmol/l), Cs+ (approximately 10 mmol/l), and Rb+ (approximately 20 mmol/l) all blocked this K+ channel reversibly. We conclude that the basolateral K+ channel of the rectal gland is distinct from other epithelial K+ channels inasmuch as it is not stimulated by Ca2+ directly, but that it is qualitatively similar to many other known K+ channels with respect to its sensitivity towards blockers.

Animals↗