Heller Ch. 2 Flashcards
What is the RMP of calcium?
+100mV (more in interstitial fluid)
What is the RMP of sodium?
+70mV (more in interstitial fluid)
What is the RMP of potassium?
-90mV (more in intracellular fluid)
What does movement of ions across a membrane cause?
A charged membrane…cations move out leaving behind negative proteins
Phase 0 of Fast Response Action Potentials?
Sodium permeability rapidly goes UP–>
a sudden DEpolarization
Phase 1 of FRAP?
Sodium permeability rapidly goes DOWN and
Potassium permeability goes DOWN–>
a slight REpolarization
Phase 2 of FRAP?
Calcium permeability goes UP
Sodium permeability slightly UP and
Potassium permeability stays LOW–>
a PLATEAU
Phase 3 of FRAP?
Potassium permeability goes UP
Calcium permeability goes DOWN and
Sodium permeability goes DOWN–>
a REpolarization (Phase 4)
Pacemaker potential cells (Slow-Response Action Potential)?
Unstable membranes
Net movement in SRAP cells before AP?
Potassium goes DOWN while
Calcium (major) and Sodium (minor) go UP–>
an eventual DEpolarization (action potential)
How is conduction velocity modified?
Connexin proteins in gap junctions
Parasympathetic actions through the vagus nerve (ACh):
An initial hyperpolarization of the RMP
Slows the rate of spontaneous depolarization of the RMP
How does ACh achieve parasympathetic effects?
ACh interacts with muscarinic receptors–>activates Gi
Increases potassium permeability (K[ACh] channels)
Suppresses adenylate cyclase–>decreased cAMP–>reduces inward-going pacemaker current by sodium (i[f] current)
Sympathetic actions (NE):
Increases inward currents carried by both sodium (i[f] current) and calcium during the diastolic interval–>increases rate of diastolic depolarization
How does NE achieve sympathetic effects?
NE interacts with beta1-adrenergic receptors–> activates Gs
Increases adenylate cyclase–> increases cAMP–> increases open-state probability of the pacemaker sodium current channel (i[f] current)
Define chronotropic:
Heart rate
Define dromotropic:
Conduction velocity
Digitalis:
Inhibits sodium/potassium pump–>decreased sodium gradient–>non-functional sodium/calcium exchanger–>increased contraction strength/length
Ryanodine:
Blocks the calcium induced calcium channel
Caffeine:
Activates the calcium induced calcium channel
Contractility:
Force at a given length
Inotropic:
Change in contractility
Tension in ventricle?
T = intraventricular pressure x internal radius
Potassium channel (inward rectifier) i[K1]
Maintains high K+ permeability during phase 4
Decay contributes to diastolic depolarization
Suppression during phases 0-2 contribute to plateau
Sodium channel (fast) i[Na]
Accounts for phase 0
Inactivation may contribute to phase 1
Potassium channel (transient outward) i[TO]
Contributes to phase 1
Calcium channel (slow inward, L channels) i[Ca]
Primarily responsible for phase 2
Inactivation may contribute to phase 3
Is enhanced by sympathetic stimulation and beta-adrenergic agents
Potassium channel (delayed rectifier) i[K]
Causes phase 3
May be enhanced by increased intracellular Ca++
Potassium channel (ATP-sensitive) i[KATP]
Increases K+ permeability when ATP is low
Potassium channel (ACh-activated) i[KACh]
Responsible for effects of vagal stimulation
Decreases diastolic depolarization and HR
Hyperpolarizes RMP
Shortens phase 2
Sodium channel (pacemaker current) i[f]
Contributes to the diastolic depolarization
Enhanced by sympathetic stimulation and beta-adrenergic agents
Suppressed by vagal stimulation
