hey guys i'm confused about the SA node and how it starts the action potential which leads to the opening of Ca2+ slow channels. Below is what I understand but I'm not sure if I completely understand it. Could someone explain this in a more simpler way? thanks!
the RMP of the SA node is -55mV. Na+ leak channels increases this to -40mV and causes a depolarization allowing the Ca2+ slow channels to open up and depolarize it even more. Then they repolarize due to K+ channels but not all the way because the SA node and Na+ leak channels generate another depolarization before the RMP is established. this creates a jagged curve/graph with sharp peaks. Also how does the curve which has the plateau of Na+-Ca2+ factor into all this? Thanks again!
Well, the SA is composed of what they call "pacemaker cells" because they spontaneously depolarize and cause action potentials to spread throughout the rest of the heart (via the internodal pathways and gap junctions between cardiac cells).
The SA node spontaneously depolarizes about 60-70 times a minute, which is what causes a normal hrt rate. The way these cells "spontaneously" depolarize, unlike normal neurons, is because of 4 special types of channels found in the heart pacemaker cells(as well as several other smooth muscle types, such as those in the intestines). Be sure to distinguish between pacemaker and contractile cells, which DO NOT depolarize spontaneously and are resp. for the actual contraction of the heart. The pacemaker cells cause the contractile cells to depolarize. Pacemaker cells are only 1% of the cells in the heart, while contractile cells are resp. for the other 99%.
The 4 special channels are:
K+ leak channels
Na+ leak channels
t-type Ca2+ channels
l-type Ca2+ channels
The process is as follows:
1. Spontaneous influx of Na+ causes the membrane to depolarize more easily, just as you said.
2. K+ channels spontaneously close (which will make it depolarize even more) and are resp. for the first rise from resting membrane potential of about -50 mV.
3. t-type Ca2+ channels are resp. for the rest of the rise/depolarization to threshold by allowing an influx of Ca2+.
4. Once at threshold, L-type Ca2+ channels cause the sharp depolarization to around +10 mV by allowing even more Ca2+ into the cell.
5. As usual, an increase in K+ permeability is resp. for the fall back to "resting membrane potential" although, it is better to visualize the graph rather than think of a "resting membrane potential" because it is constantly changing, unlike muscle cells and other nerve cells. The pacemaker cells are continually going "up" and "down" in potential, causing rhythmic contractions to travel throughout the heart, making it beat.
A graph of what this looks like is shown here:
http://upload.wikimedia.org/wikiped...tential.svg/354px-Pacemaker_potential.svg.png
To answer the second question, please don't confuse PACEMAKER cells with CONTRACTILE cells.
Contractile cells have the characteristic "plateau" phase caused by an influx of Ca2+.
Contractile cells are NOT resp. for the autorhythmicity of the heart, but the contractile activity. The contractile cell process is as follows:
1. At resting membrane potential (RMP), a rapid Na+ influx resulting from a change in voltage across the membrane causes the cell to rapidly depolarize.
2. Once it reaches the peak, a L-type Ca2+ channel influx causes the membrane to remain at this positive value for a longer period: this plateau phase stops the contractile cells to be unable to fire more than once every 250 ms, so the fastest the heart can beat is around 200 bpm.
3. Again, an increase in K+ permeability is resp. for the movement back to RMP.
Here is a good representation of that in picture form:
http://en.wikipedia.org/wiki/Image:Action_potential.png
The way certain drugs work is by changing the permeability of pacemaker cells or changing the permeability of the cell to Ca2+.
For example, Digitalis causes the heart to allow for Ca2+ in, making contractile cells contract longer due to more Ca2+ (a longer "plateau" phase). Verapamil, a Ca2+ channel blocker blocks this, essentially lessening the contractility of the contractile cells.
The sympathetic nervous system speeds up heart rate by increasing the speed at which pacemaker cells close K+ channels, hastening the rise the threshold.
Hope this helps. Jay
