Cardiac EC Coupling & Calcium Handling II Flashcards
Norepinephrine released by sympathetic nerve terminals and circulating epinephrine act to 1
Increase Heart Rate (positive chronotropy) by raising the firing rate of pacemaker cells in the SA node.
Norepinephrine released by sympathetic nerve terminals and circulating epinephrine act to 2
Increase Contractile Force (positive inotropy)
activation b-adrenergic receptors, elevation of cytoplasmic cAMP, and activation of Protein Kinase A (PKA).
Norepinephrine released by sympathetic nerve terminals and circulating epinephrine act to 3
Increase Rate of Relaxation (positive lusitropy)
activation b-adrenergic receptors, elevation of cytoplasmic cAMP, and activation of Protein Kinase A (PKA).
inotropy
an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction
lusitropy
myocardial relaxation.
Four important targets for Protein Kinase A (PKA) in cardiomyocytes are
The L-type Ca2+ channel
RyR2
Phospholamban (PLB)
Troponin
L-type Ca2+ channel
Phosphorylation of the channel increases the amplitude of the L-type Ca2+ current, increasing
(i) the trigger for activation of RyR2 and over time
(ii) the SR Ca2+ content
Phosphorylation causes PLB to dissociate from SERCA2, and thus _____________ , which speeds relaxation and increases SR Ca2+ content.
increases Ca2+ pumping into the SR
long QT, which causes the heart muscle to take longer than usual to recharge between beats.
symptoms include immune deficiency and cognitive abnormalities.
Timothy Syndrome
Linked to de novo mutations in CaV1.2
shortened Q-T interval
associated with a number of ECG alterations
linked to mutations of the cardiac sodium channel
Brugada Syndrome
______ causes the heart muscle to take longer than usual to recharge between beats.
Prolonged QT syndrome
do not display ECG abnormalities at rest, but do display abnormalities upon exercise or infusion of catecholamines.
dominant mutations in RyR2
b blockers are a standard therapy
Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT).
debilitating disorder resulting in syncope, cardiac arrhythmias and sudden death.
patients display intermittent hypoglycemia, immune deficiency and cognitive abnormalities including autism.
Timothy Syndrome
Linked to de novo mutations in CaV1.2