Help with K+ channel involvment in slowing heart rate

[monge20]

Hey, M2 receptor agonists (ACh) opens a k+ channel via a G protein (Gi, I belive).

What I don't get is how is the cardiomiocyte hyperpolarized if K+ is entering the cell?:confused:

[md90]

What I don't get is how is the cardiomiocyte hyperpolarized if K+ is entering the cell?:confused:

What conditions may keep a cardiac cell in a hyperpolarized state? the first that comes into mind are drugs such as loop diuretics,..

Is this what you mean? Are you looking for something else? Remember, the cardiac muscle is dependent on extracellular calcium for its' contraction...

[student-2]

opening K+ channels hyperpolarize cells by allowing k+ ions to LEAVE the cell. This is a very important principle to understand. Cells become depolarized due to Na+ INflux and the membrane returns to normal by k+ Efflux (out of the cell). The two ions go down their electrochemical gradient that are maintained by Na/K ATPase and membrane permeability.

[md90]

that is true, student-2,... but in cardiac cells, it is dependent on the extracellular calcium which enters during the plateau of the action potential and stimulates the sacroplasmic reticulum to release the calcium; it gives the cardiac cells:
1. plateau provided by the influx of calcium
2. spontaneously depolarize resulting in automaticity
3. electrically coupled to each other by gap junctions;

Also the calcium influx will balance the potassium efflux... not lending itself to the hyperpolarization... the question asked why is the cell in a hyperpolarized state if K+ is entering the cell... meaning that the cell is in a negative state (too many Cl- ions, not enough K+ ions,...).. I was thinking of various conditions that could lead to this... Maybe I misunderstood the question...

Please post your thoughts.. thank you

[student-2]

The question was pertaining K+ ion flow. The cardiac cell AP (both of them- pacemaker and muscle) are unique. However a common trait in the heart is that K+ flows out of the cell to repolarize the membrane. Pacemaker cells are unique in the "funny" Na+ channels that prevent a stable resting membrane potential, and the Ca2+ that begins the AP (a job usually reserved for Na+ in other cells). Cardiac myocyte APs are unique from ordinary neuron APs only in the 3rd phase in which Ca2+ enters the cell to prolong the AP duration. Furthermore this Ca2+ influx serves as a trigger to release intracellular stores of Ca2+ strengthening the cardiac contraction (ionotropy)

[md90]

thank you for the clarification... student-2... greatly appreciated

[monge20]

Parasympatic influence on heart causes ?bradycardia?, slowing of the heart rate. This is done by vagal stimulation using ACh which binds tu the muscarinic receptor M2, present in the heart. This kind of receptor is a metabotropic receptor, coupled to a G protein. When this G protein (Gi) un binds, its beta and gamma portions activate a potassium channel of the family Kir3.4 forming an IKAch (inward rectifier K+ current activated by ACh). This means ACh promotes K+ ions to ENTER the cardiac myocyte.
What I cannot understand is how can K+ entering the myocyte slow heart rate?

[student-2]

Nice explanation. However, it is physically impossible to make K+ enter a cell passively via channels due to the countering electrochemical gradient. The only way to make K+ enter a cell is by active measures which are to slow to make a change (they can MAINTAIN membrane potentials).
Furthermore, the autonomic system (sympathetic and parasympathetic) affect the heart rate at the SA and AV nodes at Ca2+ channels, not K+ channels.