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作者：Jean-Yves Lapointe, P. Darwin Bell, Ravshan Z. Sabirov, Yasunobu Okada作者单位：3 National Institute for Physiological Sciences,Okazaki 444-858 Japan; Group de Recherche enTransport Membranaire, University of Montreal, Montreal, Quebec H3C 3JCanada; and Nephrology Research and Training Center,University of Alabama at Birmingham, Birmingham, Alabama 35294
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" r$ C5 R/ ]8 b 【摘要】
3 M1 K; \& _" @3 k: `9 f% \3 d5 H Patch-clamp experiments in cell-attached (c/a) and inside-out (i/o)configurations were performed to directly observe ionic channels in lateralmembranes of macula densa (MD) cells from rabbit kidney. In the presence of140 mM KCl in the pipette and normal Ringer solution in the bath, werepeatedly observed in c/a and in i/o configurations a 20- to 23-pS channelwith a linear current-voltage ( I - V ) relationship reversingnear 0 mV. Ionic replacement in the bath solution clearly indicated a cationicselectivity but with equal permeability for Na and K .Single-channel kinetics was characterized by higher open probability atpositive membrane potentials. In i/o experiments, elimination of bathCa 2 ( 1 µM) abolished channel activity in areversible manner. This MD nonselective cationic channel was found to displaya certain Ca 2 permeability because single-channel events could be detected when the pipette potential was very negative(-60, -80, and -100 mV) in the presence of 73 mMCaCl 2 in the bath solution. The similarities between this channeland some channels of the transient receptor potential family suggest apossible role for this MD basolateral channel in controlling membranepotential and regulating Ca 2 entry during MD cellsignaling. 3 E, `9 n8 B1 S
【关键词】 transient receptor potential channels intracellular calcium patch clamp tubuloglomerular feedback nifedipine2 L0 `4 r/ q# C" o' e
THE MACULA DENSA (MD) plaque is a group of epithelial cells located in the cortical thick ascending limb (CTAL) in close proximity to thejuxtaglomerular apparatus. This constitutes a unique anatomic arrangementwhere the vascular and the epithelial networks of the kidney come intocontact. The recognized role of MD cells is to detect increases in tubularluminal fluid NaCl concentration ( L ) and transmit signals,resulting in a decrease in glomerular filtration rate (through a contraction of the afferent arteriole) and an increase in renin secretion (by the granularcells of the afferent arteriole)( 28 ). We and others haveworked toward identifying the various transport pathways expressed in MD cellsto further our understanding of the steps involved in the generation oftubuloglomerular feedback (TGF) signals. The initial step in TGF is thedetection of a rise in L by the furosemide-sensitive apicalNa-K-2Cl cotransporter ( 13, 16, 27 ), followed bydepolarization of the basolateral membrane( 2, 27 ), cellular alkalinization ( 6 ), and a modest butsignificant rise in intracellular Ca 2 concentration([Ca 2 ] i ) that is nifedipine sensitive( 25 ). Recent work suggeststhat the final transport step at the MD is the release of ATP across thebasolateral membrane and through a maxianion channel( 3 ). Whether ATP serves as thefinal mediator that elicits afferent arteriolar vasoconstriction, or if there is the requirement for the generation of adenosine, is still being debated( 28 ).0 g) r$ p* f; h6 K4 }9 j0 I4 f
4 ^9 O* _" {. c- H \( z5 V' D: bOver the last decade, substantial progress has been made in understandingthe membrane properties of MD cells, especially by applyingelectrophysiological and epifluorescence techniques ( 15 ). In previous studies, weused patch-clamp techniques to identify a K channel on the apicalmembrane of MD cells by carefully excising and removing that portion of theCTAL covering the MD apical membrane( 8 ). More recently( 3 ), we have removed the entireCTAL that surrounds the MD plaque, thereby providing an access to the lateralmembrane. Using this preparation, we now report the existence of anonselective cation (NSC) channel in MD cells that isCa 2 activated and Ca 2 permeable. This channel is proposed to play a role in the regulation of [Ca 2 ] i and basolateral membrane potential inMD cells.
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' }4 _+ A! F; SMATERIALS AND METHODS% P: i9 Q1 K+ J1 o7 T
5 S6 |2 `1 x F( f5 i; l- XTubule preparation. Studies were performed using renal tubules dissected from New Zealand White rabbits as described in previous publicationsfrom this laboratory ( 8, 12 - 16 ).Mid-CTAL with attached glomeruli were isolated by manual dissection at amagnification of x 80. The CTAL covering the MD plaque was completelyremoved, leaving the MD plaque attached to the glomerulus. This maneuverprovided direct access for patch clamping both the apical and lateralmembranes of MD cells. Free access to the lateral membrane is supported by ourprevious observation of a maxi-Cl - channel likely to beinvolved in the basolateral ATP release( 3 ). The MD-glomerulus wastransferred to an inverted microscope; a holding pipette was used to stabilizethe MD plaque and position it for access by the patch pipette. Changes in thebath solution were performed, at room temperature, using a rate of 15-20ml/min for a minimum of 45 s, corresponding 10 times the bath volume. Table 1 gives the composition of the bath and pipette solutions.# Q% g; T6 L; Z
( T8 _! h. d: z ]6 ^ @. WTable 1. Solution composition
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Patch clamping. Channel activity was recorded with standard patch-clamp techniques ( 7 )using either an Axopatch 2000 (Axon Instruments, Foster City, CA) or EPC-7amplifier (HEKA Elektronik, Lambrecht, Germany). Recordings were low-passfiltered at 2 kHz, digitized at 1 ms/point, and stored on a hard disk using acommercial acquisition system (Pclamp6, Axon Instruments). Pipettes werepulled from soft glass capillaries (Fisher Scientific, Pittsburgh, PA) using atwo-step vertical puller (model PP-83, Narishige, Tokyo, Japan) or amultiple-step horizontal puller (model P-97, Sutter Instruments, Novato, CA).When filled with pipette solution (see Table 1 ), pipette resistancewas between 2 and 5 M.In inside-out (i/o) experiments, membranepotential is reported as - V p, where V p is the pipette potential. In cell-attached (c/a)experiments, membrane potential can be estimated from- V p actual cellular potential difference. At roomtemperature, in the presence of 150 mM NaCl bath solution, this cellularpotential is expected to be quite low; an average of -25 mV in thepresence of an intact CTAL microperfused at 39°C with 150 mM NaCl haspreviously been reported ( 2, 12 ). When channel activity wasobserved, a pulse protocol consisting of 11 voltage pulses (4 s in duration)was initiated using potentials from -100 to 100 mV in 20-mV increments. In selected experiments, the mean channel activity ( NP o where N is the number of channels in the membrane patch, and P o is the channel open probability) was estimated bymeasuring the average "macroscopic" current during each 4-svoltage pulse. Leak currents were estimated from current levels recorded when all channels were closed and confirmed by observing its monotonous variationwhen the membrane potential was changed from -100 to 100 mV. Dividingthe net channel current by the single-channel current amplitude yields anestimate of NP o. Estimation of permeability ratios betweenmonovalent cations was obtained from the Goldman-Hodgkin-Katz equation. Formonovalent cations, permeability ratios( P cation / P Na ) are calculated from the reversal potential ( V R ) which is given by/ \; @7 ~' S, K, A! k
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where p and c stand for the indicated cation concentration in the pipette andon the cytosolic side, respectively, NMDG is for N -methyl- D -glucamine, and R, T, and F have their usual meaning. The permeability ratio P Ca / P Cat (where Cat stands for eitherNa or K) was evaluated from the reversal potential observed in the presence ofa high-Ca 2 concentration ([Ca 2 ]) solution on the cytosolic side and the normal pipette solution on theextracellular side (see Table1 ) using the following equation derived from the constant fieldapproximation ( 33 )
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" L7 ?: ?9 [: r# R2 ?; U+ X; rStatistics. Data are presented as means ± SE and n is the number of single-channel recordings analyzed. Statistical significanceof the difference between two means was assessed using Student's t -test for paired samples. P consideredsignificant.
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. X g* Q! H5 r% ?; N- M* l7 BDuring patch clamp of the lateral membranes of MD cells, several differentchannels were identified, including small (10-25 pS) and intermediateconductance levels (30-50 pS) as well as a maxi-Cl - channel ( 380 pS) ( 3 ). Inthe present study, we will specifically deal with a small-conductance channel (20-23 pS) that could be repeatedly seen in the lateral membrane of MDcells.
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/ M" r: I* \; |$ i$ D, PC/a mode. Figure 1 shows representative single-channel events and an average current-voltage( I - V ) curve obtained from seven c/a patches during the±100-mV pulse protocol in a normal Ringer bath. In each case, the I - V relationship was linear, yielding a mean conductance of20.6 ± 0.6 pS ( n = 7). At this stage of the experiment, carewas taken to eliminate lower conductance channels (12-16 pS) or the maxianionchannel that was sometimes observed in c/a patches. The 20-pS channel displayed a higher P o and a larger mean open time atpositive membrane potentials. In a high-K bathing solution (see Table 1 ), the I - V relationship in c/a mode remained linear (conductance =20.7 ± 0.9 pS, n = 4, data not shown) and continued to reversenear 0 mV, suggesting that the cellular potential was probably low andinsensitive to a rise in external K concentration from 5 to 80mM.
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0 r4 u4 M& P. |( |% \Fig. 1. Single-channel events in cell-attached configuration for macula densa cellsbathed in normal Ringer solution. A : single-channel recordings as afunction of minus pipette potential (- V p ). B : average single-channel current-voltage ( I - V )curve from 7 different patches. G, mean conductance.2 M% z* ?7 Y' l, l7 N
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I/o mode/selectivity. In i/o experiments, full I - V curves were obtained before and after the bathingsolution was changed from Ringer to the low-Na solution and/or tothe high-K solution (see Table1 for compositions). The single-channel conductance in Ringeraveraged 23 pS ( n = 8), and the average current reversed at 0.1 mV(see Fig. 2 ). When cytosolicNa was lowered by an order of magnitude (from 135 to 13.5 mM), the V R increased to 25.5 mV ( n = 5), indicating thatthe channel was more permeable to Na than to NMDG . The V R observed in Ringer (always with 140 mM KCl in thepipette) suggests a P K / P Na permeability ratio of 1.0. Using this value, the V R observed in the low-Na solution yields a P NMDG / P Na of 0.27. In contrast, whenthe cytosolic solution was changed from Ringer to high K , V R was displaced by only 3.5 mV ( n = 6). This isin agreement with a P K / P Na 1 anda reduction in the cytosolic Na K concentration from140 mM in the Ringer solution to 110 mM in the high-K solution(see Table 1 ). As expected froma cationic channel, reducing cytosolic Cl - by one order ofmagnitude did not affect the single-channel I - V curve( n = 4, data not shown). This 20- to 23-pS channel, with a P o that increases with depolarization, can be functionallydescribed as an NSC channel.: Y1 f, X/ _7 }- ]- b5 T
) n3 U1 X5 g( H9 W, I& lFig. 2. Average inside-out (i/o) patch I - V curves in the presenceof 140 mM KCl in the pipette. The effects of changes in the bath solution(cytosolic surface of the patch) from Ringer ( n = 8; 135 mMNa 5 mM K , ) to a low-Na solution( n = 5; 13.5 mM Na 5 mM K , ) or to ahigh-K solution ( n = 6; 80 mM K 30 mMNa , ) on the average I - V relationship areshown.; K( k2 q2 B' e' L- f; J/ x
: q4 q* l! Y ~$ }; ?) aIntracellular Ca 2 sensitivity. As shown inFigs. 3 and 4, the NSC channel requiredCa 2 on the cytosolic surface to remain active. In i/oexperiments, channel activity was completely lost on perfusion with either aCa-free (0Ca)-EGTA solution ( n = 6; pCa 8.7, assuming 2 in double-distilled water, Table 1 ) or with a 1 µM( n = 3; pCa6 solution, Table1 ). The channel could be fully reactivated when normal Ringer wasreintroduced into the bath (see Fig.3 A ). The NP o was measured in i/oconfiguration with sequential exposure to Ringer solution and alow-Ca 2 solution (either 0Ca-EGTA solution or the pCa6solution). As shown in Fig.3 B, calculated NP o values weresignificantly decreased for positive membrane potentials. Average NP o for all positive membrane potentials gave a value for NP o of 1.1 in Ringer solution that was significantly reduced to 0.16 in the low-Ca 2 solution ( P n = 5).
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Fig. 3. Reversible effect of removing Ca 2 from the cytosolicsurface on cationic channel activity in i/o patches. A :single-channel recordings as a function of the membrane potential (i.e.,- V p ) in the presence of 140 mM KCl in the pipetteand either Ringer (2 mMCa 2 )orCa 2 -free (0Ca)-EGTAsolution in the bath. Arrows indicate the 0-current level for the 3 sets oftraces. B : average (of 5 experiments) open probability of the channel( NP o, where N indicates the no. of channelspresent) as a function of - V p. Values are means± SE of 5 observations.
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Fig. 4. Channel activity during administration of 10 µM nifedipine and lowCa 2 concentration (1 µM) to the cytosolic surface ini-o experiments. A : recordings obtained from the same patchsequentially exposed to Ringer, nifedipine (a 2nd Ringer is not shown),low-Ca 2 Ringer, and then Ringer. It is shown that 1µM Ca 2 produced the same inhibition that waspreviously found with the 0Ca-EGTA solution; however, the inhibitory effectsof nifedipine were marginal. B : average NP o as afunction of - V p. The inhibitory effect of nifedipinefailed to reach statistical significance ( P = 0.11, n =4).
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Nifedipine sensitivity and divalent cation permeability. Because certain members of the NSC channel family mediate Ca 2 influx, we tested the possibility that this channel would be directly responsible for the nifedipine-sensitive basolateral pathway that mediates MD[Ca 2 ] i increase after a rise in L ( 25 ). In aseries of four i/o experiments, the presence of aCa 2 -sensitive small-conductance channel was firstpositively identified by reducing bath solution Ca 2 concentration (using either 0Ca-EGTA or the pCa6 solution) before a return toRinger solution and addtion of 10 or 20 µM nifedipine. As illustrated in Fig. 4, this largeconcentration of nifedipine failed to inactivate this channel. It was foundthat NP o was not significantly reduced by the addition ofnifedipine (see Fig.4 B ). In a consideration of all positive membranepotentials, average NP o was 1.1 in the presence of Ringersolution and decreased to 0.6 in the presence of nifedipine ( P =0.11, n = 4).0 I& d3 h; a& x: I
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To test for divalent cation permeability of the channel, we tested theeffects of a 73 mM CaCl 2 solution ( n = 4, Table 1 ). Application of the 73mM CaCl 2 solution to the cytosolic surface produced a majordecrease in NP o for both positive and negative membranepotentials (see Fig.5 A ). While a few brief openings could be detected atnegative membrane potentials (presumably K flowing from thepipette to the bath, see Fig. 5 B, trace 3 ), there were also severalsingle-channel openings, having current amplitudes of 0.6 to 1.3 pA, atmembrane potentials of 60, 80, and 100 mV (see Fig. 5 B, traces1 and 2 ). Figure 5 C, the I - V relationship forsingle-channel currents in the presence of the 73 mM CaCl 2 solutionon the cytosolic surface, shows that single-channel conductance has decreasedby a factor of 2.5. In one case ( in Fig. 5 C ),Ba 2 was used instead of Ca 2 inthe bath solution, and very similar single-channel outward currents could beobserved. In Fig. 5 C,we pooled the single-channel currents observed in five experiments and performed a linear fit of the data. In the presence of 73 mM Ca 2 (or Ba 2 ) on the cytosolicside and 140 mM K on the external surface, Eq. 2 predicts a V R of nearly -1 mV if K ions and divalent cationshave identical permeabilities. As the V R was around 9mV, P Ca / P K is estimated at 0.6.0 F6 P3 m* ?- P7 o* h
n5 e! p& n0 F `* } [; ]Fig. 5. Single-channel recording in i-o configuration with 140 mM KCl in the patchpipette and 73 mM CaCl 2 in the bath or cytosolic solution. A : recordings of 4 s in duration at different membrane potentialsfrom -100 to 100 mV. B : enlargement of the 3 portions of therecordings depicted in A ( 1-3 ). C : I - V relationship for single-channel currents (outward areCa 2 currents) obtained from single-channel eventsobserved in 5 different patches where a pulse protocol similar to the oneshown in A was used.' W# s, w4 s3 s X% l
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The present studies report the presence of a NSC channel of low conductancein MD cells that is 1 ) activated by intracellular Ca 2 , 2 ) nifedipine insensitive, and 3 ) Ca 2 permeable. The density of this channelin rabbit MD cells was relatively high because it was found in approximatelyone-half of the patches that were positive for channel activity. Beforespeculating on the role of such a channel in the physiology of MD cells, letus first compare its properties with those of similar channels found in otherepithelial cells.
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5 H+ a+ K9 G3 o8 NComparison with other NSC channels observed in epithelial cells. Low-conductance NSC channels have been reported in several tissues, includingseveral segments of the mammalian nephron, primary cultures of renalepithelial cells, and renal cell lines. Of particular interest is the 23- to27-pS NSC channel that was reported by Chraibi et al.( 5 ) in the basolateral membrane of practically all segments of the mouse nephron, from the proximal tubule tothe outer medullary collecting duct. The characteristics of this channelinclude 1 ) linear I - V curve in i/o configuration; 2 ) equal permeability to Na and K ; 3 ) NP o increase with membrane depolarization; and 4 ) requirement for channel activity in i/o configuration of 0.1 to 1mM [Ca 2 ] on the cytosolic surface. All of thesecharacteristics are compatible with the NSC channel found in MD cells.Remarkably similar channels (22- to 25-pS conductance, nonselectivity, and[Ca 2 ] i 1 µM required for channelactivation) were observed on the apical membrane of proximal tubule cells inprimary culture ( 19 ), in acortical collecting tubule cell line( 10 ), and in inner medullarycollecting duct cell lines( 18, 24, 30 ). Interestingly, in thecortical collecting duct cell lines, the NSC channel was found to be activatedby cell shrinkage ( 31 ) whereasin the inner medullary cell line these channels were activated by cellswelling ( 24 ). More recently,a cationic channel of similar conductance (22.8 pS) and poor selectivity wasreported in the apical membrane of freshly isolated outer medullary collectingduct cells of the rabbit ( 32 ).This channel appears distinct from the MD NSC channel because it was fullyfunctional in the absence of cytosolic Ca 2 (0Ca-EGTAsolution) in i/o patches. Specific roles for NSC channels are difficult toestablish, but it was suggested that NSC channels could be involved inNa reabsorption, K secretion, and volumeregulation.
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Transient receptor potential channels. Channels from the transient receptor potential (TRP) family are ubiquitously distributed and considered tobe responsible for capacitive Ca 2 entry (CCE), which isactivated after intracellular Ca 2 release. First clonedfrom Drosophila ( 22 ),the TRP gene family codes for at least 20 mammalian homologues( 4, 21, 23 ), with single-channel conductances ranging from 20-23 pS for human TRPC3( 4, 9 ) to 110 pS for the homologousTRPl proteins (TRP-like) ( 11 ). In general, these channels have poor selectivity with respect to monovalentcations, and some of them are permeable to divalent cations( 9, 20, 29, 34 ). Among the four TRPchannels expressed in the kidney, only TRPM4 codes for an NSC channel( 20 ). The functionalproperties of a splice variant named TRPM4b have been recently presented( 17 ). Northern blot analysisrevealed the presence of specific TRPM4b transcripts in various tissues, including heart, liver, pancreas, placenta, and kidney( 17 ). Interestingly, TRPM4btransfected into HEK-293 cells yields a 25-pS NSC channel with a nearly linear I - V curve and an open probability that increases with celldepolarization. This channel, which was not found to beCa 2 permeable in whole cell experiments, was activatedby agonist-induced rises in [Ca 2 ] i. Compared with measurements of membrane potential and[Ca 2 ] i in nontransfected HEK-293 cells,release of intracellular Ca 2 in transfected HEK-293cells triggers cell depolarization through the activation of TRPM4b that, inturn, causes a decrease in the driving force for Ca 2 entry. It was proposed that TRPM4b serves in the regulation of membranepotential after intracellular Ca 2 release.8 ?9 y0 K; h+ ?. S* F- J! `# F
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Putative role of the NSC channel in MD cells. A putative role forMD cell Ca 2 was considered early on in the study of TGF signal generation ( 1 ).Following contradictory reports( 26 ), the effects of changesin L on MD [Ca 2 ] i haverecently been revisited ( 25 ).It was convincingly demonstrated that MD[Ca 2 ] i increased by 40 nM when L was increased from 25 to 150 mM. In addition, this increasewas shown to be sensitive to basolateral application of 1 µM nifedipine. Itwas suggested that the basolateral membrane depolarization that occurs withelevated L ( 13 ) opens or activatesvoltage-dependent Ca 2 channels in the basolateralmembrane. Because a large concentration of nifedipine (10-20 µM) didnot completely block the MD NSC channel, this casts some doubt on whether theNSC channel is directly responsible for L -induced Ca 2 influx across the basolateral membrane. It islikely, however, that cell depolarization triggered by a rise in L will increase the P o of the NSCchannels, which will further contribute to MD cell depolarization and help inopening voltage-dependent Ca 2 channels. In the i/oconfiguration, sensitivity of NSC channels to cytosolicCa 2 1 µM Ca 2 is needed to activate the NSC channel. Because thischannel was observed to be functional in the c/a configuration, it appears that the channel's Ca 2 sensitivity is much higher inthe presence of a normal cytosolic environment compared with the excised configuration. It is possible that the NSC channel may in fact be sensitive tosmall increases in [Ca 2 ] i that have been observed when L is increased. Further experiments are neededto check for the Ca 2 sensitivity of the cationicchannel in the c/a mode and to identify a specific inhibitor that could beused to better define the role of this Ca 2 -sensitivechannel in the physiology of MD cells.
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DISCLOSURES! _1 c# D4 c9 A
8 U1 O2 I* s5 J- j9 p hThis work was supported by a Grant-in-Aid for International ScientificJoint Research from the Ministry of Education, Science, Sports and Culture ofJapan (Y. Okada), the Kidney Foundation of Canada (J. Y. Lapointe), andNational Institute of Diabetes and Digestive and Kidney Diseases GrantDK-32032 (P. D. Bell).
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ACKNOWLEDGMENTS
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9 m0 y. g7 N7 y" m* KThe technical contribution of Bernadette Wallendorf is gratefully acknowledged.0 G- d4 e& E3 M; e H
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