CV components and autoryth

Question 1

what is MDP?

Answer 1

maximum diastolic potential, -60 mV; like the RPM of autoryth cells even though they never really “rest”

Question 2

Pacemaker (SA and AV node) cells exhibit the slow response in their action potentials
i.e. AP with a sluggish rising phase

Answer 2

ya

Question 3

what is spontaneous gradual depol due to in phase 4?

Answer 3

mainly due to slow ionic influx creating the pacemaker current (funny current)

Question 4

what is the funny current caused by?

Answer 4

slow leak of Na into the pacemaker cells through Na channels which open during repolarization

Question 5

what are the three phases where ion permabilities change in pacemaker cells?

Answer 5

Phase 0, 3, and 4

Question 6

describe phase 4 ion permeability changes

Answer 6

slow leak of Na into the cell causing the funny current; K efflux also rapidly decreases due to the closing of vg K channels; opening of transient Ca channels during the last half of the pacemaker potential—> Ca influx; net result: more positively charged membrane

Question 7

describe phase 0 ion permeability changes

Answer 7

opening of L-type Ca channels (vg) after reaching threshold (-55 mV)–> rapid influx of Ca; no fast Na channels involved–> therefore, no quick upwards slope like in contracile myocyte APs;

Question 8

describe phase 3 ion permeability changes

Answer 8

begins with gradual closing of vg-Ca channels (Ca influx stops); vg-K channels activate–> efflux of K (rapid)–> repol; once MDP is reached, Na channels open again

Question 9

what variable influence cardiac rhythmicty (HR)?

Answer 9

1. Rate of diastolic depol; 2. MDP; 3. Threshold potential

Question 10

how is rate of diastolic depol changed?

Answer 10

sympathetic stimulation can INCREASE it by releasing NE–>higher Na and Ca influx–>steeper slope –> increased HR
ACh can also decrease slope of phase 4–> decrease in HR

Question 11

how is MDP change?

Answer 11

release of ACh by the parasym NS; induces hyperpol–increased efflux of K, decreased influx of Ca; –> MDP becomes more negative, takes longer to reach threshhold–> decrease in HR;

Question 12

how is threshold potential altered?

Answer 12

via antimalerial and antipyretic (fever) drug quinidine–>shifts threshold voltage towards zero (makes more positive)–>takes longer to reach threshold–>increase in HR–>bradycardia