Overview SA Node Action Potential; also AV Node Phase 0, upstroke action potential opens L-type voltage-gated Ca2+ channels secondary to T-type voltage-gated Ca2+ channels further depolarizing cell membrane enough to reach threshold for L-type votage-gated Ca2+ activation → upstroke slope of upstroke is slower than other cardiac myocytes due to lack of large Na+ currents in SA and AV nodal cells due to non-rapid Ca2+ movement via channels Phase 1 and 2 are absent in SA node action potential Phase 3: repolarization voltage-gated K+ channels open → ↑ K+ conductance → outward K+ current → repolarization Phase 4: diastolic depolarization accounts for automaticity of SA node cells to generate an action potential spontaneously without neural input hyperpolarization-activated cyclic nucleotide-gated (HCN) channel generates "funny" current (If) repolarization activates HCN channels non-selective monovalent ion channel evokes Na+ mediated depolarization If slow depolarization activates T-type voltage-gated calcium channels reduced outward K+ current contributes to depolarization Heart rate set by the rate of depolarization in phase 4 ↑ rate of phase 4 depolarization → reach threshold faster → ↑ action potential per unit time by SA node cells → ↑ heart rate pharmacology correlate sympathetic nerveous system stimulation → ↑ heart rate norepinephrine acts on β1 receptors in SA node → ↑ If → ↑ rate of phase 4 depolarization → ↑ heart rate example of a positive chronotropic effect parasympathetic nervous system stimulation → ↓ heart rate acetylcholine acts on M2 receptors in SA node → ↓ If → ↓ rate of phase 4 depolarization → ↓ heart rate also ↑ K+ conductance → ↑ outflow K+ current via K+-ACh receptors an example of a negative chronotropic effect
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