| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Laboratory of Ocular Physiology and Biochemistry, Department of Optometry and Radiography, The Hong Kong Polytechnic University, Hung Hom, Hong Kong.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionReferences |
|---|
METHODS. Fresh isolated bovine CBE was mounted in an Ussing-type chamber. The effects of ion substitution and transport inhibitors on electrical measurements and Cl transport were investigated.
RESULTS. The potential difference (PD) across the preparation was 0.55 ±
0.04 mV and was consistently negative at the aqueous side. The
short-circuit current (SCC) and tissue resistance
(Rt) were found to be 8.0 ± 0.7
µA/cm2 and 72 ± 3 
/cm2,
respectively. Both the PD and the SCC of the bovine CBE were found to
depend primarily on the concentration of the Cl bath and to a lesser
extent on the Na or HCO3 concentration. At 30 mM Cl, the
polarity of the PD and the direction of the SCC were reversed. Reducing
the extracellular Na or Cl concentration abolished the net Cl transport
into the eye under the short-circuited condition. Bilateral bumetanide
(0.1 mM), but not 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid
(DIDS; 0.1 mM), greatly inhibited the Cl transport. Bumetanide, when
applied to either side, inhibited the Cl transport. The effect,
however, was three times greater on the stromal side than on the
aqueous surface. Bilateral heptanol (3.5 mM) and
5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB; 0.1 mM) on the
aqueous side also inhibited the Cl transport by 80% and 92%,
respectively.
CONCLUSIONS. The results suggest that the major Cl influx pathway at the basolateral border in pigmented epithelial cells is through the Na-K-2Cl cotransporter, but not the Cl/HCO3 and Na/H double exchangers. Intercellular gap junctions between the two cell layers and the NPPB-sensitive Cl channels at the basolateral surface in nonpigmented epithelial cells also play a crucial role in regulating the Cl movement across the functional syncytium.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
Earlier studies demonstrated active Cl secretion across the ciliary body of cat,4 toad,5 and rabbit,6 although a subsequent study questioned the presence of any active Cl secretion.7 Our recent study demonstrated the active Cl transport in bovine CBE, which may be important in aqueous humor formation.8 To allow for transepithelial Cl transport to occur across the ciliary epithelium, at least three transport steps are involved: 1) loading of Cl from ciliary stroma into the PE cells through the stromal basolateral surface, 2) passive diffusion of Cl through the gap junctions into the NPE cells, and ultimately 3) efflux of Cl from NPE cells to the posterior chamber.9 10 A number of cotransporters, ion exchangers, ion channels, and NaK-adenosine triphosphatases (ATPases) have been identified in the ciliary epithelium, which may facilitate the vectorial Cl transport across the functional syncytium.11 12 13 14 15 16 Currently, two major mechanisms for the uptake of Na and Cl at the basolateral surface in PE cells have been hypothesized3 (Fig. 1) . One of the mechanisms is through a bumetanide-sensitive Na-K-2Cl symport, and the other mechanism is through a parallel Cl/HCO3 and Na/H double exchange. Because most of these transporters and ion channels have been characterized only in cultured ciliary epithelial cells, their roles in transepithelial ion transport and their contributions to aqueous secretion are yet to be determined.
|
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
Figure 2 illustrates the PD-sensing device used in our experiments. Essentially, it consisted of two potential-sensing tubes that were connected to each other by a by-pass arm through three-way stopcocks. At the beginning of the experiment, both the potential-sensing tubes and the by-pass arm were filled with normal Ringer (NRR) solution. The potential sensing tubes were then fitted into the PD-sensing arms of the chamber. By switching the three-way stopcocks to position A, any junction potentials between the 0.9% NaCl and Ringer solutions or associated with the Ag/AgCl electrodes could be nullified. The stopcocks were then switched back to position B to allow the measurement of the electrical parameters across the preparation in the chamber. At that point, the fluid junction was exactly the same as in position A (0.9% NaCl and Ringer solutions). The offset potential was checked frequently with the by-pass arm and stopcocks throughout the experiment.
|
Measurement of Radiolabeled Cl Flux
In the initial experiments, after a brief stabilization period,
Ringer solution with a particular drug was perfused to the preparation
until its full effect on the SCC was demonstrated. Later, a
radiolabeled (hot) solution with that drug was perfused and allowed to
equilibrate before the flux measurements, as described
earlier.8
In the subsequent experiments, we loaded the
drug together with the hot solution and skipped the drug-only
treatment. The results were not different from those before, and the
electrical parameters remained stable throughout the experiments.
The unidirectional Cl fluxes were determined under the short-circuited conditions. To minimize the variability between individual eyes, only those data from paired measurements (i.e., using the same eye) were compared. This was achieved by mounting two preparations from each eye: One preparation was for the measurement of influx (Jsa: stroma-to-aqueous), and the other preparation was mounted in another identical chamber for backflux measurement (Jas: aqueous-to-stroma). The net flux was the difference between Jsa and Jas. In other words, a single net flux data point was obtained from each eye. After a 60-minute equilibration period, perfusates from both half chambers were collected separately with two scintillation vials. The samples were taken from each side at 12-minute intervals until a stable flux was obtained. The radioactivity of all the samples was measured with a liquid scintillation counter (Wallac 1414 Winspectral DSA; Wallac, Helsinki, Finland) after the samples were mixed with 15 ml of a biodegradable scintillation cocktail (Amersham Radiochemicals, Amersham, UK).
For the sake of calculation, the net Cl flux
(J) can be converted to the SCC by using the
following equation:
 |
Pharmacologic Agents in Ringer Solution
In the Na substitution experiments, the Na concentration in the
Ringer solution was reduced to 24 mM (the control Na concentration
being 136 mM) by exchanging it for an equimolar amount of choline or
N-methyl-D-glucamine (NMDG). In
reduced Cl and HCO3-free media, the Cl and
HCO3 were similarly replaced by equimolar amounts
of gluconate or cyclamate.
The radiolabeled isotope of [36Cl] was purchased from Amersham Radiochemicals. Other pharmacologic agents used were: 3-[aminosulfonyl]-5-[butylamino]-4-phenoxybenzoic acid (bumetanide), 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid (DIDS), 5'-(N,N-dimethyl)-amiloride hydrochloride (DMA), and dimethyl sulfoxide (DMSO; all from Sigma, St. Louis, MO); 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB; BIOMOL Research, Plymouth Meeting, PA); and heptanol (Fluka Chemie, Buchs, Switzerland). All these chemicals were dissolved in DMSO before they were added to the Ringer solution. The final concentration of this solvent in the Ringer solution was adjusted to 0.1%. Preliminary experiments showed that DMSO has no effect on the electrical parameters and Cl flux (data not shown).
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
/cm,2
respectively. These electrical parameters
remained stable for 4 to 5 hours. Both the PD and the SCC were found to
be higher than those in our previous report. This may have been due to
an improvement in the mounting technique. The effects of ion
substitutions on the electrical parameters are summarized in Tables 1
and 2
. The polarity and magnitude of the PD and the SCC were found to
depend primarily on the concentration of Cl in the solution. At 60 mM
Cl, when the Cl was replaced by gluconate, the PD was immediately
abolished, and the SCC was reduced by approximately 95%. Reducing Cl
to 30 mM even reversed the polarity of the PD. In a similar experiment
shown in Table 3
, cyclamate replaced Cl in the solution. The sequential reduction of Cl
in the solution on both sides also produced a stepwise decline in the
PD and SCC. This finding is comparable to results shown in Tables 1
and 2
. In experiments with either reduced Na concentration or
HCO3-free media, inhibition of the PD and the SCC
was also observed. However, the inhibitory effect was less drastic than
that of when Cl was reduced, and a negative PD was preserved. The
effects of ion substitution on the electrical parameters were
reversible, except in HCO3-free media in which an
incomplete recovery was seen.
|
|
|
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
Our result was different from those in the studies by Kishida et al.17 and Krupin et al.18 who reported a positive PD in rabbit ciliary body under HCO3-free conditions. The reason for the difference is not fully understood, but variations in the ion transport between different species have been proposed.17 21 It is interesting to note that those species (e.g., rabbits) that have an excess of HCO3 in aqueous humor compared with plasma have a corresponding deficit of Cl in aqueous. The reverse is true for humans.22 In cattle, the Cl concentration in aqueous is also found to be higher than that of plasma, as in humans, although no information is available for HCO3 concentration. The high concentration of HCO3 in the rabbit’s aqueous is thought to be for buffering the acids produced by the anaerobic respiration of the relatively large crystalline lens.23 From this point of view, it is likely that the mechanisms of transepithelial Cl and HCO3 transport in the ciliary epithelium are different between species, as reflected in the difference in ionic dependence.
Mechanisms of Transepithelial Cl Transport
Chu and Candia7
have found that the calculated
conductance of Na and Cl is larger than the measured conductance,
suggesting the presence of electrically coupled Na and Cl transport.
Because the SCC is equal to the algebraic sum of all ion transport
processes, the current generated from the transepithelial Cl transport
can therefore be larger than the measured SCC if complex ionic
transport activities are involved. Our results indicate that the
measured SCC was only approximately 30% of the net Cl flux, suggesting
that much of the Cl movement across the ciliary epithelium took place
in an electroneutral manner. We tried to look at the Na8
and HCO3 (unpublished observation) fluxes but
failed to show a significant net transfer to account for the apparent
discrepancy between the SCC and the Cl fluxes. The exact ion-coupling
mechanism remains unclear. However, as the unidirectional Na fluxes are
several times larger than the Cl fluxes, even in the absence of net Na
transport, we cannot rule out the possibility of coupled NaCl
transport.8
In the present study, we therefore tried to
reduce the Na concentration in the solution to see whether it would
affect the electrical parameters and unidirectional Cl transport. The
Na concentration in the solution was reduced to 24 mM, which is
approximately the intracellular Na concentration in most epithelial
cells,24
including rabbit ciliary epithelial
cells.25
This maneuver was expected to dissipate the
driving force for Cl uptake, if any, into the PE cells.
It has been documented that the NaK-ATPase at the basolateral border in PE cells creates a substantial transmembrane Na gradient3 and favors the intracellular accumulation of Cl in ciliary epithelium.26 Provided that the transepithelial Na and Cl transport was independent but in the same direction, reducing the Na concentration would inhibit Na transport solely and should result in a hyperpolarization due to the predominance of Cl transport. However, we found that reducing the Na concentration in the soltuion depolarized the PD and decreased the SCC. These results imply that Cl may couple with Na in transepithelial transport. Total inhibition of the net Cl influx under reduced Na concentration confirmed the importance of extracellular Na in the Cl transport process. The coupled movement of Na and Cl in the PE cells was achieved by using the Na gradient maintained by the NaK-ATPase.1
The coupled movement of Na and Cl may be achieved in many different ways, such as through Na-K-2Cl symport or by parallel Na/H and Cl/HCO3 antiport. These two mechanisms are not mutually exclusive. It is possible that both mechanisms work simultaneously, although one or the other mechanism may be more pronounced in a given species. A recent study of rabbit ciliary epithelium in which an Ussing chamber was used has shown that the SCC was inhibited by both bumetanide and DIDS, suggesting that both the Na-K-2Cl symport and the Cl/HCO3 antiport contribute to the net ion fluxes across the ciliary epithelium.27
Na-K-2Cl Cotransport System
Wiederholt and Zadunaisky26
and Weiderholt et
al.28
demonstrated the inhibitory effect of loop diuretics
on both the SCC and the intracellular Cl activity in shark ciliary
epithelium. Edelman et al.29
subsequently analyzed the
volume of isolated PE and NPE cells which were subjected to anisosmotic
perturbations and transport inhibition. They have suggested that
bumetanide-sensitive Na-K-2Cl cotransport constitutes the principal
pathway for ion entry into the PE cells. In the present study,
bumetanide caused a significant inhibitory effect on both electrical
measurements and Cl secretion. The transepithelial Cl transport was
inhibited by 85% to 90% when bumetanide was added to both sides. More
than 60% of this inhibition (54% of 86%) can be explained by the
effect exerted on the stromal surface. We also noted an 18% inhibition
of Cl flux when bumetanide was applied to the aqueous side (data not
shown). The reason for this is not clear. Evidence for the presence of
Na-K-2Cl cotransport has been reported in human NPE
cells.30
Crook and Riese31
have proposed that
Na-K-2Cl cotransporter may be present at the apical borders of NPE
cells and may provide an additional pathway for Cl entry into the NPE
cells. A more recent study on rabbit ciliary epithelium has even
suggested that Na-K-2Cl cotransporter may be present at the basolateral
membrane in NPE cells, enhancing the Cl transport into the aqueous
humor.32
The exact mechanism remains to be determined. Our
findings indicated that a bumetanide-sensitive Na-K-2Cl cotransport is
present primarily at the basolateral membrane in PE cells and
contributed to the transepithelial Cl movement in bovine ciliary
epithelium.
It is worth noting that when bumetanide was applied to the stromal side, it not only inhibited the influx, but also stimulated the backflux. This phenomenon also applied to some other experimental conditions such as bilateral heptanol. The exact reason is not known. An early study of toad CE has suggested that Cl backflux was entirely a passive and diffusional flux.5 However, a later report has indicated that in addition to the secretive pathway, there is a reabsorptive pathway through which Cl can be returned to the stromal side.33 There are many ion transporters present on the surface of the NPE cells, which can regulate the "active" ion reabsorption into the functional syncytium. We speculate that in normal secretion of aqueous, the cotransporter works in such a way that it dominates the directional influx of Cl across the ciliary epithelium by driving the Cl out of the cells into the posterior chamber. However, when the cotransporter in the PE cells is blocked (as with bumetanide), the influx decreases and the intracellular Cl concentration drops accordingly. Owing to the decrease in the directional driving force of Cl, the reabsorption of Cl increases to replenish the intracellular Cl. In that case, the Cl backflux is increased because more Cl is returned into the stroma. A new equilibrium is ultimately reached when the influx and backflux are similar in magnitude.
Cl/HCO3 and Na/H Antiport System
Evidence for the role of Cl/HCO3 and Na/H
exchangers in ion transport across the ciliary epithelium have been
presented in the literature: a reduction of extracellular
HCO3 concentration abolished the net Cl influx in
rabbit6
; Cl uptake was stimulated by an outwardly directed
HCO3 gradient on cultured bovine PE
cells13
; both PE and NPE contained more Cl when incubated
with HCO3-rich media32
; and recovery
of intracellular pH of the rat’s ciliary epithelial cells from acid
load was dependent on the presence of external Na and was inhibited by
amiloride, whereas pH recovery from alkali load was inhibited by either
replacement of external Cl or inclusion of DIDS.34
Such
evidence supports a model of Cl/HCO3 antiport
working in parallel with an Na/H exchanger, which together mediate the
uptake of Na and Cl into the functional syncytium. Na and Cl were
exchanged for H and HCO3. The intracellular pH
and carbonic anhydrase indirectly governed the double-exchange
mechanism. Our results show that bilateral DIDS (0.1 mM) significantly
decreased the SCC by half, but interestingly it had no effect on the
unidirectional Cl flux in either direction. The reason for this
phenomenon is not clear. We suggest that the correlation between the
electrical parameter measurements and ion fluxes is not simple,
possibly because of the complex syncytial structure of the ciliary
epithelium. The SCC reflects the summation of all electrogenic
activities across this bilayered structure; however, the exact ionic
components contributing to the SCC have yet to be elucidated. Until the
whole picture is known, the contribution of Cl transport to the SCC
will remain unclear. Simultaneous abolishment of electrical
measurements and Cl flux was seen in some of the experimental
conditions, such as with aqueous NPPB and bilateral heptanol. However,
with 60 mM Cl, the electrical parameters were greatly inhibited, but a
substantial portion of Cl flux remained. Krupin et al.35
suggested that a change in the SCC does not necessarily permit the
identification of any change in solute transfer. Further study may be
required to clarify the relationship between the Cl flux and the SCC in
the ciliary epithelium.
In theory, DIDS may have inhibited 10% to 15% of Cl flux that was not inhibitable by bumetanide (86% inhibition). However, this amount of inhibition may not be easily identified with an Ussing-type setup. We therefore suggest that Cl/HCO3 may play a minor role in transepithelial Cl transport. It is possible that DIDS acted on other electrogenic pathways, which may have been involved in housekeeping functions, such as the regulation of intracellular pH.12 36 This pathway remains unknown and awaits further experimentation.
Our results were in contrast to those reported by McLaughlin et al.32 on rabbit ciliary epithelium. They proposed that the dominant entry pathway of NaCl uptake is through a parallel Cl/HCO3 and Na/H antiport based on the measurements of ion contents in the PE and NPE cells. Although different species and methodologies were adopted, the exact reason for the discrepancy is unknown and remains to be elucidated.
Gap Junctions
The PE and NPE cells are joined at their apical membranes by gap
junctions,2
which allow free passage of ions from the PE
cells to the NPE cells. Similar ionic contents between PE and NPE cells
have been demonstrated by electron-probe x-ray
microanalysis,25
suggesting the existence of highly
effective communication between the two cell layers. Our results
indicate that bilateral 0.05% heptanol (equivalent to approximately
3.5 mM) inhibited both electrical parameters and net Cl flux by
approximately 80%. This was in agreement with a rabbit study in which
the SCC was inhibited by 85% to 90% with 3 mM
heptanol.37
This concentration has been shown not to
interfere with other cellular functions except for the uncoupling of
junctional communication.37
Our finding suggests that much
of the Cl movement across the ciliary epithelium is through a
transcellular pathway rather than a paracellular route. We noted a 7%
to 8% decrease in Rt after bilateral heptanol,
the exact reason for this decrease is not clear. It is possible that
heptanol has other physiological effects on the paracellular pathway,
such as loosening the tight junction. Further studies are required to
verify this hypothesis.
Cl Efflux
The efflux of Cl into the posterior chamber has been suggested to
play an important role in aqueous secretion.9
Intracellular accumulation of Cl was found in the NPE cells of
shark26
and rabbit25
above its
electrochemical equilibrium, therefore driving the passive movement of
Cl from the NPE cells to the posterior chamber through the Cl
channel.10
38
The role of Cl channel or related conductive
pathways in aqueous secretion have been documented: Cl channel blockers
such as NPPB39
40
and DIDS39
41
42
were shown
to inhibit the regulatory volume decrease of canine and transformed
human NPE cells; changes in membrane potential of NPE cells induced by
extracellular Cl substitution15
and ß-adrenergic
stimulation42
could be prevented by DIDS; and currents
activated by hypotonic solution in patch clamping can be prevented by
pretreatment with NPPB and DIDS.43
In the present study,
the differential SCC response of NPPB on the stromal and the aqueous
sides indicates the NPPB-sensitive Cl conductive pathway is present
predominantly at the NPE cells. It has been shown that NPPB may have
other effects such as blocking the K channel.44
However,
blocking the cation conductance at the aqueous side should induce
hyperpolarization rather than depolarization of the PD as observed when
NPPB was added to the aqueous surface. Potassium channel blocker
BaCl2 (1 mM) at the aqueous side resulted in a
substantial hyperpolarization and did not affect the inhibitory effect
of NPPB on the PD and the SCC (Table 7)
. However, it was difficult to affirm the specificity of NPPB on Cl
channel in our setup definitively. It indicated that NPPB blocked
primarily the anion, possibly the Cl channels, but not the K channel.
The inhibition of Cl transport by aqueous NPPB indicated that the Cl
channel is the major efflux pathway into the aqueous humor.
|
|
Conclusion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
|
Footnotes |
|---|
Submitted for publication December 15, 1998; revised July 21 and December 29, 1999; accepted January 7, 2000.
Commercial relationships policy: N.
Corresponding author: Chi-Ho To, Laboratory of Ocular Physiology and Biochemistry, Department of Optometry and Radiography, The Hong Kong Polytechnic University, Hung Hom, Hong Kong. orchto{at}polyu.edu.hk
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  M. Shahidullah, C.-H. To, R. M. Pelis, and N. A. Delamere Studies on Bicarbonate Transporters and Carbonic Anhydrase in Porcine Nonpigmented Ciliary Epithelium Invest. Ophthalmol. Vis. Sci., April 1, 2009; 50(4): 1791 - 1800. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. S. Law, O. A. Candia, and C.-H. To Inhibitions of Chloride Transport and Gap Junction Reduce Fluid Flow across the Whole Porcine Ciliary Epithelium Invest. Ophthalmol. Vis. Sci., March 1, 2009; 50(3): 1299 - 1306. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Selvam, P. B. Thomas, H. J. Gukasyan, A. S. Yu, D. Stevenson, M. D. Trousdale, A. K. Mircheff, J. E. Schechter, R. E. Smith, and S. C. Yiu Transepithelial bioelectrical properties of rabbit acinar cell monolayers on polyester membrane scaffolds Am J Physiol Cell Physiol, October 1, 2007; 293(4): C1412 - C1419. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Y. Chan, J. A. Guggenheim, and C. H. To Is active glucose transport present in bovine ciliary body epithelium? Am J Physiol Cell Physiol, March 1, 2007; 292(3): C1087 - C1093. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. A. Candia, C.-H. To, and C. S. Law Fluid Transport across the Isolated Porcine Ciliary Epithelium Invest. Ophthalmol. Vis. Sci., January 1, 2007; 48(1): 321 - 327. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-W. Kong, K.-K. Li, and C.-H. To Chloride Secretion by Porcine Ciliary Epithelium: New Insight into Species Similarities and Differences in Aqueous Humor Formation Invest. Ophthalmol. Vis. Sci., December 1, 2006; 47(12): 5428 - 5436. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. R. Calera, H. L. Topley, Y. Liao, B. R. Duling, D. L. Paul, and D. A. Goodenough Connexin43 is required for production of the aqueous humor in the murine eye J. Cell Sci., November 1, 2006; 119(21): 4510 - 4519. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. W. Do, K. Peterson-Yantorno, and M. M. Civan Swelling-activated cl- channels support cl- secretion by bovine ciliary epithelium. Invest. Ophthalmol. Vis. Sci., June 1, 2006; 47(6): 2576 - 2582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. A. Candia, C.-H. To, R. M. Gerometta, and A. C. Zamudio Spontaneous Fluid Transport across Isolated Rabbit and Bovine Ciliary Body Preparations Invest. Ophthalmol. Vis. Sci., March 1, 2005; 46(3): 939 - 947. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. W. Do, W. Lu, C. H. Mitchell, and M. M. Civan Inhibition of Swelling-Activated Cl- Currents by Functional Anti-ClC-3 Antibody in Native Bovine Non-Pigmented Ciliary Epithelial Cells Invest. Ophthalmol. Vis. Sci., March 1, 2005; 46(3): 948 - 955. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-W. Do, C.-W. Kong, and C.-H. To cAMP Inhibits Transepithelial Chloride Secretion across Bovine Ciliary Body/Epithelium Invest. Ophthalmol. Vis. Sci., October 1, 2004; 45(10): 3638 - 3643. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-W. Do, K. Peterson-Yantorno, C. H. Mitchell, and M. M. Civan cAMP-activated maxi-Cl- channels in native bovine pigmented ciliary epithelial cells Am J Physiol Cell Physiol, October 1, 2004; 287(4): C1003 - C1011. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Wu, K. Yao, J. Flammer, and I. O. Haefliger Role of Anions in Nitric Oxide-Induced Short-Circuit Current Increase in Isolated Porcine Ciliary Processes Invest. Ophthalmol. Vis. Sci., September 1, 2004; 45(9): 3213 - 3222. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Shahidullah, W. S. Wilson, M. Yap, and C.-h. To Effects of Ion Transport and Channel-Blocking Drugs on Aqueous Humor Formation in Isolated Bovine Eye Invest. Ophthalmol. Vis. Sci., March 1, 2003; 44(3): 1185 - 1191. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Y. Avila, R. W. Seidler, R. A. Stone, and M. M. Civan Inhibitors of NHE-1 Na+/H+ Exchange Reduce Mouse Intraocular Pressure Invest. Ophthalmol. Vis. Sci., June 1, 2002; 43(6): 1897 - 1902. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Z. Ellis, J. A. Nathanson, J. Rabe, and K. J. Sweadner Carbachol and Nitric Oxide Inhibition of Na,K-ATPase Activity in Bovine Ciliary Processes Invest. Ophthalmol. Vis. Sci., October 1, 2001; 42(11): 2625 - 2631. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. W. McLaughlin, D. Peart, R. D. Purves, D. A. Carre, K. Peterson-Yantorno, C. H. Mitchell, A. D. C. Macknight, and M. M. Civan Timolol may inhibit aqueous humor secretion by cAMP-independent action on ciliary epithelial cells Am J Physiol Cell Physiol, September 1, 2001; 281(3): C865 - C875. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-H. To, C.-W. Do, A. C. Zamudio, and O. A. Candia Model of ionic transport for bovine ciliary epithelium: effects of acetazolamide and HCO3- Am J Physiol Cell Physiol, June 1, 2001; 280(6): C1521 - C1530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. K. Wetzel and K. J. Sweadner Immunocytochemical Localization of NaK-ATPase Isoforms in the Rat and Mouse Ocular Ciliary Epithelium Invest. Ophthalmol. Vis. Sci., March 1, 2001; 42(3): 763 - 769. [Abstract] [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
