channels
- ionotropic; e.g., Na, K channels
- metabotropic; e.g., beta receptors
electrochemical equilibria = membrane potential that would keep any ion at its observed concentration inside and outside
-example; if K channels open the membrane will become hyperpolarized to its equilibrium potential which is - 95 mv. this is how most inhibitory neurotransmitters work.
Ohm's Law I = V/R where I = current; V=voltage; R=resistance
Rectifying currents deviate from Ohm's law; i.e., current is not linear with voltage.
- inward
- outward
Conduction velocity = f(rate of change of voltage) - substances that block Na channels will slow conduction; e.g., high potassium; cocaine
Action potentials
slow cells - pacemaker cells
T type Ca channels activation by hyperpolarization
L type by depolarization
Another good figure below and explanation (from Lilly)
The maximum negative voltage of pace-maker cells is approximately -60 mV, substantially less negative than the resting potential of ventricular muscle cells (-90 mV). The persistently less negative membrane voltage of pacemaker cells causes the fast sodium channels within these cells to remain inactivated.
fast cells (myocytes; purkinje fibres)
this is a very helpful figure to understand fast action potentials:
Here is another way to understand ion currents in the fast action potential:
From Lilly; Pathophysiology of Heart Disease. Schematic representation of a myocyte action potential (AP) and relative net ion currents for Na+, Ca++, and K+. The resting potential is represented by phase 4 of the AP. Following de-polarization, Na+ influx results in the rapid upstroke of phase 0; a transient outward potassium current is responsible for partial repolarization during phase 1; slow Ca++ influx (and relatively low K+ efflux) results in the plateau of phase 2; and final rapid repolarization largely results from K+ efflux during phase 3.
myocardium = .3-1 m/sec
av node = .02 - .1 m/sec (important to allow time for filling of ventricles)
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