Cardiovascular Flashcards
2 Types of cardiac muscle cells
Contractile: striated, branched, sarcomere-containing with small fibers
Contain intercalated disks, with anchoring desmosomes and gap junctions through which electrical signals flow
Spiral arrangement of muscle to contract apex → base
Compared to skeletal muscle have larger T tubules and smaller ER bc they receive some Ca2+ from ECM
**Pacemaker: ** smaller, autorhythmic, myogenic cells without organized sarcomeres
Pacemaker potential = unstable resting member potential containing funny channels (If) permeable to K+ and Na+ causing RMP drift
Calcium induced calcium release in contractile cardiac cells:
AP moves through sarcolemma down t tubules and opens voltage-gated Ca2+ channels, Ca from ECM (10%) opens RyR CICR channels on SR → stored Ca released (90%) into sarcoplasm
Ca removed by Ca-ATPase into SR and ALSO 3 Na-Ca (1) exchanger (NCX) into ECM
Skeletal muscle contraction review (same in contractile cardiac)
Ca binds troponin C to pull tropomyosin away → actin binding site open → myosin head release Pi and swivels → to pull actin towards M line → ADP is released (rigor state) → ATP binds myosin head and relaxation to cocked position occurs
Phases 0-4 of contractile cardiac cell AP
Ion channels in a pacemaker AP
Explain the role of the autonomic divisions in control of heart rate.
The intrinsic rate of the SA node is 90-100 bpm
Tonic parasympathetic control (ACh on M receptors) reduces resting heart rate
↓ decrease in ACh release can increase HR
Beyond 100 bpm, sympathetic (NE on β1 receptors) can increase HR more
Phospholamban
Regulatory protein in contractility
Catecholamines → cAMP → phosphorylation of phospholamban which ↑ Ca-ATPase activity in SR - makes more Ca available for release during CICR
More Ca = active crossbridges = ↑ force of contraction (force ∝ # active crossbridges)
Respiratory pump
inspiration ↓ pressure in inferior vena cava drawing more blood into it from abdominal veins
Myogenic autoregulation
Vascular smooth muscle in arterioles self-regulates state of contraction based on mechanically gated stretch receptors which stimulate contraction
Contraction increases R to reduce blood flow to the area (Flow = ∆P/R)
Hypoxia, active hyperemia and reactive hyperemia
Hypoxia = Low O2 + High CO2 + H+ in interstitial tissue → NO release by endothelium (vasodilator to increase blood flow)
Active hyperemia = Low O2 + high CO2 from state of metabolic activity → β2 vasodilation
Reactive hyperemia = increase in blood flow to an area following low blood flow
Chemicals Mediating Vasoconstriction and Vasodilation (3 each)
Vasoconstrict:
1) NE (⍺ receptors): baroreceptor reflex, sympathetic NT
2) Endothelin: local control blood flow, vascular endothelium, paracrine
3) 5-HT: released by activated platelets, NT
Vasodilate:
1) Epinephrine (β receptors), blood flow, adrenal medulla, neurohormone
2) NO: local control blood flow, endothelium, paracrine
3) Histamine: blood flow increase, mast cells, paracrine
