Talk:Inward-rectifier potassium channel

Question
I do not believe the above description of inward rectifing pootassium channel is correct. The correct one is this: when a cell potential enters hypopolirization (the potential is more negative then its resting potential), there are 'inward potassium rectifiers' that allow K to enter the cell making the cells potential more positive and bringing it to its normal resting potential. — Preceding unsigned comment added by 132.70.50.117 (talk • contribs) 20:46, 11 November 2006 (UTC)


 * The description in the article is correct. Kir channels can also mediate depolarizing currents in the situation you allude to (though you might want to learn to spell), but it's important to not give people the impression that Kir channels mediate the K+ mediated repolarization current following action potential initiation (mediated instead by Kv). --Dpryan 00:01, 13 November 2006 (UTC)

question
Is this sentence right?: "Thus in cells with a -60 mV resting potential, these channels would be inactivated at membrane potentials greater than -40 mV."

I thought that they close - that means that they were blocked by spermine or mg2+ - at -70 mV. -70 mV is +20 mV over the K+-equilibrium potential of -90 mV. At -90 mV the flux of K+ is zero and when the flux of k + is getting more, mg2+ or spermine is carried along into the channel and the channel is blocked. But at a resting potential of -60 mV the conductance of Na+ is such high that on the other side the conductance of K+ out of the cell is high, too. That means that at a resting potential of -60 mV is not achieved.

Well thats what I found on other sites in the internet....is that right? 80.144.202.70


 * I've reworded that sentence to be less confusing. What I assume the original author (wasn't me) meant was that for a K+ reversal potential of -60mV then Kir channels would largely be blocked at -40mV. -60mV isn't what all of us were taught to be the K reversal potential, but it can happen, for example, in muscle. Of course, this is all a generalization since some Kir channels are only weakly rectifying (e.g., Kir1 family) and could still conduct significant current at more depolarized potentials...but it's probably not best to deluge the reader so early on with such details. BTW, you may want to be more careful with the usage of the word "close". I, and likely others, consider "plugged" channels to be blocked, not closed. Kir channels can also close and this process doesn't depend on voltage or intracellular polyvalent cations...but of course that's pretty nit-picky. --Dpryan 19:06, 20 March 2007 (UTC)

new question
hi, it's me again...on some webpages you can read that there are kir-channels in neurons with a resting potential of -70 mV. Is that right?, because I always thought that the resting potentials of neurons (-70 mV) is determined by a flux of Na+ - Ions in the 'background' and that this flux is responsible for the higher resting potential. The Na+ - flux results in a K+ - flux out of the cell, too, but that would mean that the kir-channels are blocked at this resting potential. But with blocked K+ - channels there is no resting potential possible. I hope you know what I mean. or is there a difference between weakly ones and the 'normal' ones? I didn't find more information about kir-channels in neurons on the internet, so i ask you and hope that you know a answer to my little problem. 80.144.218.94
 * You're over-simplifying the makeup of the membrane. Remember that there are transporters (perhaps this is what you meant by background) and chloride channels in the membrane as well. It's safe to say that sodium channels contribute only a negligible amount to the resting potential (RMP) of a normal neuron (though in some diseases this may not be the case). Of course, at more depolarized potentials the contribution of Kir channels to the RMP is decreased markedly, but there is still a small contribution. At these potentials the importance of the Cl- reversal potential is increased. Always keep in mind that there are a lot of different kinds of channels and transporters in the membrane and that it's the contribution of all of these that results in the RMP.


 * On a related note, you can observe a wide range of RMPs in different tissues. I've seen -30mV RMPs in spastic smooth muscle.--Dpryan 18:30, 23 March 2007 (UTC)

Suggestion
I think it would be really nice to include a couple figures in this article detailing the Current-Voltage relationship in the inwardly rectifying K+ channel. In the article by Dhamoon & Jalife (J Heart Rhythm, 2005), the first Figure demonstrates the current-voltage relationship very well. comcc (talk) 23:16, 5 December 2008 (UTC)


 * The figure in the article actually show the same information as the figures in that paper, though I guess the ones in the paper you referenced are more immediately understandable to the lay reader. The next time I do recordings I'll run a ramp protocol and post it as a figure, unless someone else already has one sitting around of course. --Dpryan (talk) 05:32, 6 December 2008 (UTC)

Ins and outs
There have been edits here bordering (almost, not quite) on edit wars, so I thought I'd put some explanation here and let anyone who disagrees explain their thoughts below. Inward currents (measured in voltage-clamp) are, well, inward, in that positive charge goes into the cell. The whole positive/negative thing gets very confusing, admittedly, but inward currents are "positive." Furthermore, they are (even more confusingly!) conventionally graphed as downward deflections of the current (not the voltage, which is clamped!). That's what the page says now. If anyone disagrees, please explain here. --Tryptofish (talk) 21:12, 7 February 2009 (UTC)


 * I doubt anyone disagrees, I expect that the edits you refer to are vandalism. BTW, nice clarification that you added in your most recent edits, I agree that this is confusing to a lot of people (especially since Hodgkin & Huxley did it differently in their original papers). --Dpryan (talk) 00:11, 8 February 2009 (UTC)
 * ...And I just realized that I borked things with my edit by not reading carefully, thanks for fixing things...silly me. --Dpryan (talk) 00:17, 8 February 2009 (UTC)
 * Thanks! --Tryptofish (talk) 20:23, 8 February 2009 (UTC)

Dear Tryptofish and Dpryan, The recent edits were not the act of vandalism. I am a medical student currently taking physiology and believe your convention is mistaken(or at the very least, outdated). In common convention, the resting cell membrane potential is at around -60 mV, with potassium equilibrium potential at -80mV and ENa at 60mV. An equlibrium potential is defined as the electrical force needed to exactly counterbalace the current due to the concentration gradient of an ion. During an action potential, Na flows into the cell (depolarization), while K flows out of the cell (repolarization). Since the equilibrium potentials of Na and K are positive and negative, respectively, their currents must be negative, and positive. By convention, the flow of positive ions into the cell is a negative current, while the flow of positive ions out of the cell is a positive current. You even contradict yourself a few lines below the disputed paragraph where it says: "when the membrane potential is clamped below the channel's resting potential (e.g. -60 mV), negative current flows (i.e. positive charge flows into the cell)" It seems as if we're really just arguing over semantics here. The definition of positive vs. negative current simply depends on whether the inside or the outside of the cell is taken as ground. However, by the widely accepted norm of the action potential being represented as a rise in membrane potential, with the repolarization being represented as a decline in membrane potential, Na flowing into the cell is a negative current, while K flowing out of the cell is positive current. I've consulted my physiology professor, who agress with this statement. Please let me know if you still disagree... —Preceding unsigned comment added by Shershko (talk • contribs) 03:46, 10 February 2009 (UTC)
 * Dear Shershko: Thank you very much for your thoughtful explanation. (And I have to add an aside that I am absolutely delighted that you, as a student, have taken so much interest in this subject. Less so for your physiology prof, though. Not that it's really relevant, but I'm a long-time physiology prof myself, and one with multiple major research grants on inwardly-rectifying K+ channels, and your prof is dead wrong.) Actually, I never really thought the edits were vandalism, but you are right when you describe this matter as one of semantics, and there is a convention followed in electrophysiology, so I want us to get it right. Let me take what you have said from the bottom up. Yes, an action potential is a rise in membrane potential, but that is voltage, not current. We do indeed define the cell interior (somewhat arbitrarily) as negative relative to the exterior ground, but that means that a current such as an inward Na+ current makes the interior of the cell more positive (less negative), and thus, it is a positive current. So, when positive charge moves into the cell from outside, that's a positive, inward current. Positive charge moving out is a negative, outward current. When you say the article (not me, I didn't write that part) contradicts itself a few sentences later, you are right! (I hadn't read that far, was just reverting what I guess were your changes in the first paragraph.) At Vm more negative than ErevK, there is an inward current (which is graphed as a downward deflection in the figure), so I'm going to change that from "negative" to "inward," which I think (hope) is less confusing and more to the point. "Typical" K+ currents (such as those that repolarize after an action potential) are outward currents, unlike those discussed in this page. Your discussion of resting potential and reversal potential is correct, but, again, please remember that those are voltages, not currents. Please reply with any critiques or skepticism about what I wrote here; admittedly, it's dense. And I hope you continue to bring your enthusiasm and interest both to this subject and to WP. --Tryptofish (talk) 20:38, 10 February 2009 (UTC)

Thanks for the response, Tryptofish, but I still have some issues with your reasoning. iNa = -CdV/dt on the upstroke of the action potential, which demands that the inward current have a negative sign. Also, if inward currrent is to be below the abscissa, it must have a negative sign. Otherwise Ohm's Law gives a negative slope, which is impossible. —Preceding unsigned comment added by Shershko (talk • contribs) 00:50, 11 February 2009 (UTC)
 * In the equation you wrote, I'm not clear where you got the negative sign, or how one would determine capacitance for these purposes. See: Capacitance for what I think is the equation you mean; in practice, I don't know anyone who uses it in electrophysiology. The origin of the (admittedly kludgy) convention of displaying current the way it is done (in a raw recording, not an I-V graph) has very little to do with being intuitively attractive, and everything to do with how the recording headstage output is displayed on an oscilloscope when switching from a voltage recording to a current recording. I realize that these explanations are not very satisfying from the point of view of being intellectually consistent, but they are conventions that have been followed pretty consistently within the field, and they pre-date me. --Tryptofish (talk) 20:15, 11 February 2009 (UTC)


 * You're likely used to seeing that equation written as $$I_{ionic} + I_{capacitance} + I_{stimulation} = 0$$, so at a point where there's 0 stimulation and the only notable current is via sodium channels you get the equation with the negative sign that Shershko wrote. According to Hille (Ion channels of excitable membranes, 3rd edition, page 8) we can attribute the whole naming nomenclature to Benjamin Franklin. Having said that, I can probably count on one hand the number of times I've ever seen that used, as pretty much everyone talks in terms of how things are graphed and measured. So, no one would say in a paper when describing the graph from the main article, "The positive current (-5nA) at -60mV driving force...". People actually follow the (to quote Hille again) "...convention [that] outward membrane currents always are considered positive..." which is focused on the value and how things are graphed. I would actually suggest the article be changed to refer to values and perhaps a footnote mention the (largely) obscure naming convention, since that will help avoid confusion (this also matches more closely how I and (seemingly) others are taught, since I only vaguely remember the Franklin derived nomenclature being mentioned in passing). --Dpryan (talk) 23:45, 11 February 2009 (UTC)

Thanks, Devon, for articulating what I was trying to explain. I agree that the article should be changed to the widely accepted convention (positive ions flowing outward=positive current, represented by a downward deflection in the action potential graph). Which one of you would like to go ahead and change it? —Preceding unsigned comment added by Shershko (talk • contribs) 03:51, 12 February 2009 (UTC)
 * Well, if we agree on anything, it's that this article is in need of some rewriting in the interests of clarity (someone else can start). However, I would suggest dropping the whole positive/negative thing in favor of inward/outward. --Tryptofish (talk) 23:13, 12 February 2009 (UTC)

Great Edit, Tryptofish! It is much clearer now. I think it might still be helpful to also address the downward vs. upward deflection. I recognize that an inward flow is represented as a negative deflection on the oscilloscope, but the upward deflection of the action potential on the membrane potential vs. time graph is more relevant. Perhaps it might even be beneficial to replace the current figure with an action cardiac action potential curve, seeing how an oscilloscope recording means very little to those who have never used one in a physiological context before. My guess is that the majority of people who wiki membrane channels are college or medical students, where the oscilloscope is never discussed. What do you think? —Preceding unsigned comment added by Shershko (talk • contribs) 05:17, 13 February 2009 (UTC)
 * Thank you. I'm glad that helped. A big part of the point you raised here has to do with the difference between voltage clamp and current clamp recordings. As a quick partial fix, I added a phrase linking to the voltage clamp page, which may help point confused readers in the right direction. Of course a real explanation of voltage versus current clamp, or of action potentials, or of cardiac electrophysiology, does not belong in this article, but instead in several others. When I have more time than I do now, I will look into adding some "see also" links on this page. Also, when I have more time, I think it will help to explain here how inward rectification differs from the more "traditional" and familiar outward rectification. --Tryptofish (talk) 19:18, 13 February 2009 (UTC)
 * I've now made a bunch more edits along these lines, and I hope they help. By the way, I went back and re-read what Hille said about Ben Franklin, and that was only to the effect that "positive current flows in the direction of movement of positive charges." Nothing about neurons there; one would be forced to call both inward and outward currents (of cations) "positive" by that train of thought, which would be nonsense. But I've steered clear of positive/negative in favor of inward/outward in the article, just to avoid that sort of confusion. --Tryptofish (talk) 20:05, 22 February 2009 (UTC)

SUggestion:
I think the way that you present inwardly rectifying K channels is confusing here because it is not clear from what is written that the term "inwardly rectifying" comes from when the membrane potential is artificially made more negative then the equilibrium potential of Kir channels (-90mV) where by they open and produce a large inward current. As opposed to most other channels that are "outwardly rectifying" in that they open at depolarizing potentials. The thing that you did not make clear in your article is that physiologically these channels never let K+ "into" the cells. They are responsible for maintaining the negative resting membrane potential at around -60mV to -80mV, which they accomplish by letting K+ leave the cell. I repeat, There are no cells in the body (with the exception of hair cells in the Organ of Corti) that let K+ into the cytoplasm without the expenditure of ATP (Na/K ATPase). THus, Kir channels only let K+ flow out of the cells. THis is a point of utmost importance to stress as it was a very confusing point for me when I learned about Kir channels and maintence of the RMP.

66.230.10.218 (talk) 20:26, 16 August 2009 (UTC), CHris
 * Hi Chris, thank you for your interest. I don't know where you learned that, but it is somewhat incorrect. Although it is true that membrane potential rarely becomes more negative than the K+ reversal potential under physiological conditions, these channels do carry inward K+ currents when it does. Although so-called "weak" inward rectifiers can carry a measurable outward current, "strong" rectifiers do not. To some extent, you are confusing inward rectifiers with leak channels. Thank you for pointing that out, and I will try to revise the page to clarify it. --Tryptofish (talk) 20:45, 16 August 2009 (UTC)

Tryptofish, I've done some more research and yes you are right that Kir channels do carry more inward current (into the cell) when the resting potential (RMP) becomes more negative then the equilibrium potential of K (EK = -90mV). Additionally, the primary contributors to the RMP are actually two-pore (K2P) channels. Thanks for pointing this out. However, in support of my point that Kir channels actually carry "outward" current to help stabilize membrane potential are supported by the following:

"Under the appropriate electrochemical potentials they (the Kir channels) conduct more inward than outward potassium current. However, the conditions necessary to drive inward current fluxes are rarely met in animal cells. Thus, despite their name the principal physiological currents Kir channels conduct are outward potassium currents." (Cell, Vol. 96, 879–891, March 19, 1999, Copyright 1999 by Cell Press Transmembrane Structure of an Inwardly Rectifying Potassium Channel.Daniel L. Minor, Jr., Susan J. Masseling, Yuh Nung Jan, and Lily Yeh Jan*)

http://cvri.ucsf.edu/~dminor/pdf/03_19_99.pdf

Further, there are some specific examples given in the book Medical Physiology 2nd edition by Boron and Boulpaep:

One Kir subfamily, the G-protein activated inwardly rectifying K+ channels (GIRKs) is regulated by the Betagamma subunits of heterotrimeric G proteins. These channels are present in cardiac tissue. When acetylcholine binds muscarinic receptors in the heart the Betagamma subunit diffuse to neighboring GIRK channels and activates their opening. "The resulting increase in outward K+ current hyperpolarizes the cardiac cell, thereby slowing the rate at which Vm approaches the threshold for firing aaction potentials and lowering heart rate".

Thus, my point is that you should not down play the Kir channels physiological role, which as you can see is primarily to hyperpolarize cells that they are present in by allowing K+ efflux at negative membrane potentials. I urge you to make changes in your article that stress the physiologic role of the Kir channels. I have had to rediscover this over and over. I hope this helps. Thank you. —Preceding unsigned comment added by 66.230.10.218 (talk) 21:26, 17 August 2009 (UTC)
 * Thanks. It is helpful to see what is and what isn't clear to readers. I've made some changes in hopes of addressing that. --Tryptofish (talk) 19:32, 18 August 2009 (UTC)
 * Tryptofish, let me know if my recent edit confuses things. I can also simply swap out that figure for one with a ramp protocol (http://www.dpryan.com/Rectification.png) if it'll make things less confusing for the lay reader. --Dpryan (talk) 21:23, 19 August 2009 (UTC)
 * Thanks for correcting the error I made. In my opinion, it is easier for the lay reader to understand the figure that is there now, rather than the I-V curve, so I wouldn't change images. But I'm confused about something: it looks like the current is reversing (0 current) at 0 mV, rather than at a typical Erev for K+. (That was the reason I made the edit that I did.) If the K+ is not isotonic, then is RMP for this kind of cell near 0 mV? --Tryptofish (talk) 21:49, 19 August 2009 (UTC)
 * Wait a minute, I went back and re-read your edit summary. So external [K+] was 30 mM? So does that mean the cell was depolarized to around 0 mV? --Tryptofish (talk) 21:53, 19 August 2009 (UTC)
 * More like -30 or -40mV. You get a bit larger current with 30mM external K so your signal to noise is nicer in recordings versus when using physiological K levels. The voltage steps are then relative to the holding potential, which is whatever the resting membrane potential happens to be (should be Erev). Some people prefer showing driving force (as in the figure currently in the article) while others prefer absolute voltages (as in the one I linked to above). If you're expecting one and get the other then you can become very, very confused! --Dpryan (talk) 23:30, 19 August 2009 (UTC)
 * OK, good, so just to make sure I've got this straight: there is enough of a resting K+ current that resting membrane potential is approximately equal to the K+ reversal potential; thus, the holding potential in the experiment is also close to Erev. Is that correct? --Tryptofish (talk) 13:30, 20 August 2009 (UTC)
 * Yep, you are exactly correct. --Dpryan (talk) 21:03, 20 August 2009 (UTC)
 * Whew! How many PhDs does it take to screw in a light bulb? :) Thanks! --Tryptofish (talk) 21:07, 20 August 2009 (UTC)

Rectification Overview edits
I just undid some of the edits recently done by an anon editor. Some of them were helpful, which I kept. I should note the main reasons: Hopefully that explains things better than a terse edit summary. --Dpryan (talk) 01:53, 1 December 2009 (UTC)
 * Open/closed state isn't really affected by voltage; intracellular polyvalent cation blockage is voltage (actually driving force) dependent.
 * Voltage and current clamp were swapped. I fixed that, and removed the bit about current clamp since it wasn't really relevant to that section.
 * Thanks. I made some further changes. --Tryptofish (talk) 23:22, 2 December 2009 (UTC)

Figure 1
Just to understand the downward deflections shown in figure 1: Cause there's still a current flowing into the cell at a voltage-clamp greater than -60 and even -20mV. Assuming the reversal potential of -60mV (see article), there should be an outward driving force to K+ at potentials more positiv than -60mV. That makes one believe that under this (experimental conditions) the reversal potential of K+ is near -10mV. Is that right!? --Andykolandy (talk) 11:28, 1 March 2010 (UTC)
 * Yes, you are correct. This is a somewhat confusing aspect of this figure. The explanation for why the reversal potential is not more negative is that an artificially high external concentration of K+ was used for the experiment (to make it easier to see the Kir currents). There is more discussion on this point, under just above. --Tryptofish (talk) 16:23, 1 March 2010 (UTC)

Many thanks:), especially for the quick reply!! --Andykolandy (talk) 17:33, 1 March 2010 (UTC)

HCN Pex5R
I'll just leave this here — Preceding unsigned comment added by Niubrad (talk • contribs) 07:12, 4 May 2010

Repolarization
Another med student here learning about physiology and trying to wrap my head around all the different K+ channels (as they are important for the diagnosis of the different long QT syndromes.) Many of my resources (papers, texts, professors) seem to agree that IK1, in addition to allowing for inward K+ current and blocking outward current at more positive potentials, does contribute to repolarization of the human cardiac action potential. The way that this article reads seems to be really diminishing their influence on both repolarization and resting potential. Trypotofish, you appear to be a very knowledgeable resource and I was hoping you could speak to this. I included a passage of a review paper that I recently read to show you one resource where I was getting this notion. The wiki page on the cardiac action potential also seems to agree. Thanks so much.

"The fact that the strongly inwardly rectifying IK1 channels conduct at negative membrane potentials suggests that these channels will play a role in establishing the resting membrane potentials of Purkinje fibers, as well as of atrial and ventricular myocytes. Direct experimental support for this hypothesis was provided with the demonstration that ventricular membrane potentials are depolarized in the presence of Ba2+, which blocks IK1 channels. In addition, action potentials are prolonged, and phase 3 repolarization is slowed in the presence of extracellular Ba2+, suggesting that IK1 channels also contribute to repolarization, particularly in the ventricular myocardium. The voltage-dependent properties of IK1 channels, however, are such that the conductance is low at potentials positive to approximately -40 mV. Nevertheless, because the driving force on K+ is markedly increased at depolarized potentials, these channels should contribute outward K+ current during the phase 2 plateau and during phase 3 repolarization."

http://physrev.physiology.org/content/85/4/1205.full.pdf+html Physiol Rev October 2005 vol. 85 no. 4 1205-1253

I understand how their decreased conductance upon depolarization contributes to prolonged depolarization, but I don't understand why their role in bringing the membrane closer to K+ resting potential in the later stage of repolarization (cardiac AP phase 3), and why their role in holding the cell at resting potential (phase 4) is so diminished. Perhaps this is just an issue of the verbage of the article, am I just reading too far into the distinctions the article is trying to make? Or am I just missing something else that matters much more? —Preceding unsigned comment added by 165.124.124.155 (talk) 21:36, 9 February 2011 (UTC)


 * The passage that you quoted is talking about the membrane potential changes that were measured in the presence of Ba2+, which should block these channels (but unfortunately will also block a lot of others), so I'm not exactly sure what you are referring to in your questions, particularly what you mean by "so diminished" (by what?) in phase 4. But I would expect these channels to mediate a small outward (hyperpolarizing) current that could contribute to the negative shift in membrane potential during phase 3, and could also contribute to the resting potential in phase 4. Put another way, during phase 2, the depolarizing Ca2+ current is much larger than the hyperpolarizing K+ current, whereas the opposite is true during phase 4. Does that help? If not, please let me know.


 * Is there something in this article (ie, the one here in Wikipedia) that is confusing in this respect? Just fyi to you and to whoever else will come along in the future, this talk page is really about how to improve this article, whereas questions about the subject matter should really be asked at Reference desk, although I'm happy to try to answer questions if I can. --Tryptofish (talk) 01:10, 10 February 2011 (UTC)


 * Sorry, sometimes my questions get so verbose that the point that I am trying to make gets lost. As I read this article, especially the third and fourth paragraph of 'Overview of inward rectification', I get the sense that these channels play little if any role in repolarization and in sustaining the resting potential. It is my understanding that the role they play in repolarization and in sustaining the resting potential in myocytes is actually quite substantial. I wanted to see if that was true or if I was mistaken, and if I am not mistaken I was planning on rewording or adding some statements to reduce the confusion of future readers who might come to this page when trying to learn more about cardiac electrophysiology.Rkoz24 (talk) 04:08, 10 February 2011 (UTC)
 * Oh, OK, I see what you mean. Now here, I have to say that my background is as a neuroscientist, not as a cardiac physiologist, and I'm afraid that this is an instance in which those of us with PhDs can be overly specialized! I'm actually not that familiar with which channels are in cardiac tissue. To the best of my knowledge, what this page says in those paragraphs, and what it says lower down in the box about cardiac myocytes, is basically correct. Also, there are "strong" inward rectifiers, which mediate very little outward current, and "weak" inward rectifiers, which mediate somewhat more, so, to the extent that there are weak inward rectifiers in cardiac cells, they could play such a role (or, for that matter, a very high density of expression of strong rectifier molecules could probably do the same). I just did a quick read of the Physiol Rev review that you linked above, and I think that it is consistent with what I just said: the authors treat Kir as contributing to those processes, but not mediating them exclusively or even primarily. (It might not be clear, but Ba2+ blocks multiple kinds of K+ channels.) So cardiac phases 3 and 4 are mediated by a variety of K channels, including but not at all limited to the Kirs. The G protein coupled K channels activated by muscarinic cholinergic receptors (vagus nerve) are also inwardly rectifying. Bottom line, this is something where things are not absolute, and it's not the case that one particular channel subtype accounts for the whole thing, so these channels can contribute, but only as a part. If there's a good source for saying the role is different in the heart than in neurons, I'd be all in favor of adding that to this page. --Tryptofish (talk) 22:58, 10 February 2011 (UTC)

Slowing membrane repolarization
"Kir channels close upon depolarization, slowing membrane repolarization and helping maintain a more prolonged cardiac action potential."

How would Kir slow the repolarization if its in a closed state? Just to make sure I'm on the same level with everyone else here: Kir enables diffusion of potassium into the cell? Repolarization is the membrane potential getting negative...back to its -75 to -85 mV in cardiac cells?

Can anyone explain to me now, how disabling the diffusion of potassium (= positive charge) into the cell (= making the cell more positive = polarization of the zell = the opposite of repolarization) slows down(!) the repolarization? I just dont see how this makes any sense.

--80.121.5.166 (talk) 19:13, 3 May 2013 (UTC)
 * It's correct as written, but admittedly it can be confusing. Please think of it this way. Kir channels carry an inward K+ current, but only at membrane potentials that are more negative than the potassium reversal potential. When the cardiocyte is depolarized, the membrane potential is less negative than the potassium reversal potential. For that reason, any open K+ channels will carry K+ ions out of the cell, making the membrane potential more negative (less positive charge inside). Thus, if Kir channels were open under depolarized conditions, they would act (along with most "typical" K+ channels) to repolarize the membrane during the latter part of the action potential. But Kir channels don't do that, because they close (or are blocked) when the membrane depolarizes. Consequently, a possible outward K+ current isn't there, and the action potential can last longer than it would have if the current had been there. --Tryptofish (talk) 21:49, 3 May 2013 (UTC)


 * Very well. That makes the name inward rectifier highly confusing though. EDIT: Because the parasympathetic nervous system acts on the sinoatrial node and atrioventricular node over a Kir as well (GIRK1) activating it via acetylcholine. The currents that flow over this channel and mediate a negative chronotropic and negative dromotropic effect, are both outward potassium currents...flowing through an inward rectifier. Yes you have faster repolarization and a negative inotropic effect through GIRK1 as well, but that plays almost no role, because you only get that in the atrium and contraction of the atrium doesnt have a that big role in heart function, cause if it would you wouldnt be able to live with atrial fibrilation. tl;dr this confusing naming really rustles my jimmies --77.117.246.55 (talk) 09:22, 4 May 2013 (UTC)
 * Yes, I understand that. But of course Wikipedia works with the names for things that the outside world has given us. Thanks. --Tryptofish (talk) 21:08, 4 May 2013 (UTC)

Question on thermodynamic principles of inward rectification
Hello,

I am a biochemistry major undergrad, and I was wondering if anyone could explain (and perhaps this would make for a good edit in the article itself) the following points about rectification:

To my understanding (and sources like: http://arxiv.org/ftp/arxiv/papers/1112/1112.2363.pdf), channels are akin in function to enzymes. How is it then that rectifier channels can seemingly do what no enzyme can - allow the reaction to approach equilibrium from one side (excess external K+) faster than from the inside (excess cytosolic K+)? Even my textbook (Stryer, Biochemistry, 7th ed., ch. 14 question 10) says that an ion channel must transport in both directions with the same rate. If channels really lower the activation barrier energy which should accelerate both directions of transport equally, how does rectification exist while not messing up the thermodynamics? What are good ways or analogies to think about these channels - are they like leaky diodes?

Also, do the topological features of these proteins (like the large funnel-like opening towards the cytosol and the vestibule, and the - charged nature of the residues facing the cytosol) affect the rectification, or do these factors only do the enzymatic function/work both ways?

Thanks! — Preceding unsigned comment added by CallousGallus (talk • contribs) 04:28, 1 March 2016 (UTC)


 * I also wondered about this. I would guess (!) that they are like leaky diodes, i.e. they only let potassium pass along an existing potential which would deliver the needed Gibbs energy. 2003:C9:D710:D703:67EE:BF91:D704:B3C2 (talk) 12:12, 28 November 2023 (UTC)

Assessment comment
Substituted at 06:23, 7 May 2016 (UTC)