Page 52 - Cardiac Nursing

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28 PA R T I / Anatomy and Physiology

■ Figure 1-25 Schematic diagram
showing extracellular and intracellular
calcium cycles that control cardiac
excitation–contraction coupling and
relaxation. Major structures and cal-
cium “pools” (bold capital letters).
(From Katz, A. [2006]. Physiology of
the heart [4th ed., p. 194]. Philadel-
phia: Lippincott Williams &
Wilkins.)

Calcium exerts some effects by combining with the intracel- membrane protein by cAMP creates a conformation or pore diam-
lular protein calmodulin. In cardiac myocardial cells, the eter change that places the calcium channel in a functional state
calcium–calmodulin complex promotes calcium ion binding to available for voltage activation. 54 cAMP may also facilitate the SR
troponin and thus promotes contraction. Calcium–calmodulin release of calcium. Both actions promote an increased cytosolic cal-
also may stimulate calcium ion pumps on the SR and sar- cium concentration and thus promote muscle contraction.
colemma and may stimulate sodium–calcium exchange; these Phospholamban is an SR membrane protein that activates the
actions help remove calcium ion from the cytosol. Calcium– SR calcium pump. Phosphorylation of phospholamban by cAMP
calmodulin influences the synthesis and breakdown of cAMP and by calmodulin at a different site stimulates the calcium pump,
and may promote sarcolemmal calcium influx. Calcium may increases SR calcium uptake, and promotes relaxation. cAMP
exert several other effects, either directly or by combining with phosphorylation of troponin influences the interaction between
other intracellular proteins, and thus may modulate myocardial troponin and calcium, and promotes relaxation.
cell contraction and relaxation through several different mech- Although calcium ion uptake into the SR promotes relax-
anisms. ation, mechanisms increasing the amount of calcium ion in the
Stimulation of -adrenergic receptors on the cardiac cell mem- SR cause increased calcium ion availability for tension genera-
brane influences transmembrane calcium fluxes and cardiac con- tion during subsequent contractions. Thus, the increased rate
traction through the intracellular production of cAMP from ATP. and strength of contraction produced by -adrenergic stimula-
cAMP in turn initiates several reactions involving intracellular pro- tion and other combined chronotropic–inotropic mechanisms
tein phosphorylation (transfer of high-energy phosphates) by pro- appear to be matched by mechanisms that enhance the rate of
tein kinases. Phosphorylation of a sarcolemmal calcium channel cardiac relaxation. 54