Cardiac Muscle
thin = acTIN
thick = myosin
cross bridge = myosin globular head + actin - MEDIATED BY TROPONIN C-ACTIN
inside myocyte
- CICR - CONTRACTION ryanodine receptor (blocked by dantrolene in malignant hyperthermia)
- SERCA - RELAXATION
- Na - Ca exchanger - relaxation = Ca extrusion from cell
- Ca atpase = relaxation
- phase 3 - reduced Ca influx
ca channel blockers affect cardiac muscle but not skeletal - why?
ANS regulates heart rate
actual HR of 60 but intrinsic HR (all ANS receptors blocked) = 110 due mainly to PNS dominance
ANS regulates contractility
SNS increases via Gs
cAMP PKA
- ca influx
- phosphorylates ryanodine receptors
- phosphorylates phospholamden = increased serca = faster relaxation
PNS
- inhibits sns pathways via Gi
- inc. Kach channel = hyperpolarize
signal transduction pathways in heart
RV cardiac (Qp) output always equals LV cardiac output (Qs) unless there is an intracardiac shunt. If right to left shunt is present Qs > Qp. If left to right shunt is present, Qp > Qs. more on this to come.
RV cardiac (Qp) output always equals LV cardiac output (Qs) unless there is an intracardiac shunt. If right to left shunt is present Qs > Qp. If left to right shunt is present, Qp > Qs. more on this to come.
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