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12 Cards in this Set

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SMC membrane:
receptors
channels
RMP
*stretch receptors open with tension and allow a depolarizing influx of Na+ and Ca++
*VOCC open upon depolarization
*VO-K+ open to repolarize
*RMP set at -45mV by Na+/K+ ATPase and Na+ and K+ leak channels
Action of vasodilators on SMC
*B-2 AR agonists, adenosine, and PG cause increased cAMP
*NO, histamine, and bradykinin cause increased cGMP
*cAMP and cGMP cause opening of K+ channels which repolarizes membrance and closes VOCC
*cAMP and cGMP also cause increased action of Ca++ efflux pumps
*[Ca++] decreases and relaxation occurs
Action of vasoconstrictors on SMC
*a-AR agonists, angiotensin II, and vasopressin bind G-protein
*G-protein: liberates IP3 which causes release of Ca++ from SR; causes closure of K+ channels which depolarizes the membrane and opens VOCC
*increased [Ca++] results in phosphorylation of myosin and contraction
sympathetic innervation of cardiac myocytes
1. NE or epi bind B-1 AR which activates adenylate cyclase to increase [cAMP]
2. cAMP activates PKA
3. PKA causes increased opening of VOCC during systole and less inhibition of SR Ca++ pumps during diastole
intercalated disks
*adherens junctions and desmosomes allow the cells to contract as a sheet
*gap junctions allow passage of ions and thus an AP between cells
Differences between cardiac and skeletal muscle (3)
*in cardiac muscle the max amount of Ca++ is not released thus CTY can be graded
*in cardiac muscle, performance is graded by changes in PL, HR and CTY
*skeletal muscle does NOT use extracellular Ca++ for contraction
Ways to increase [Ca++] in cardiac myocytes
(4)
*increase extracellular [Ca++]
*increased opening of VOCC
*increased number of VOCC
*inhibition of Ca++ efflux pumps
What happens during relaxation at diastole?
*VOCC and ryanodine channels close
*Ca++ is extruded and returned to SR by primary active transport (ATPases) and secondary active transport (Na+/Ca++ antiporters)
What happens during relaxation at diastole?
*VOCC and ryanodine channels close
*Ca++ is extruded and returned to SR by primary active transport (ATPases) and secondary active transport (Na+/Ca++ antiporters)
Excitation-contraction during systole...where does the Ca++ come from?
*AP causes VOCC on cell surface to open and allow an influx of Ca++
*AP on T-tubule causes release of Ca++ from the SR
*activity of VOCC can be modulated by physiology, drugs, or disease
Parasympathetic innervation of heart
*preganglionic fibers begin at the medulla and synapse at visceral ganglia, where they release ACh that binds nicotinic receptors on the postganglionic neuron
*postganglionic fibers travel to the atrial wall, the SA node, and the AV node where they release ACh that binds muscarinic receptors
*action is decreased HR, CTY, and conduction velocity
*NO ventricular action
SNS innervation of heart
*preganglionic fibers begin at T1-T6 and synapse at the cervical ganglia or sympathetic trunk where they release ACh that binds nicotinc receptors on the postganglionic fibers
*postganglionic fibers travel to the atria, ventricles, SA node, and AV node where they release NE that binds B-1 receptors
*action: increase HR, CTY, and conduction velocity