Review of Neural Control of the Cardiovascular System

Within the CNS, two primary centres control CV function.
Cardioacceleratory Centre -- Mediated by the sympathetic nervous system, beta and alpha-one receptors activate this system while alpha-2 autoreceptors will inhibit sympathetic outflow from the CNS. This area is the origin of peripheral sympathetic control of CV function.

Cardioinhibitory Centre -- Mediated by the parasympathetic nervous system, this centre serves as the origin of peripheral parasympathetic control of CV function.  Effects are mediated by cholinergic muscarinic receptors.

NOTE that these centres may either increase or decrease in activity as a reflex action in response to changes in pressure that may be detected by baroreceptors in the atrium, aortic arch, carotid sinus, and elsewhere throughout the body.  Additionally, chemoreceptors may also regulate the specific activity of these centres as well as other areas of the brain that control urine output, blood volume, and other factors that may indirectly influence cardiovascular function.
 

Peripheral Control
Cardiac Control
Sympathetic system -- Primarily beta-1 receptors control the heart.  Activation of these receptors at the SA node, AV node, and directly on myocardium (particularly the ventricular myocardium) will result in increased force and rate of contraction (positive inotropic and positive chronotropic effects).

Parasympathetic system -- Activation of muscarinic receptors (innervated by the vagus nerve) at primarily the SA and AV nodes will result in negative chronotropic and inotropic effects.  NOTE that this is the breaking system of cardiac control.  If the parasympathetic control were not present, the heart would be in a constant state of overstimulation.

Vasculature -- The vascular is predominantly controlled by the sympathetic system.  HOWEVER, parasympathetic activity may influence vessels.
Sympathetic system -- Activation of alpha-1 and alpha-2 receptors will cause vasoconstriction.  Beta-2 activation will result in vasodilatation.

Parasympathetic system -- Muscarinic receptor activation will result in vasodilatation EXCEPT in coronary vessels where constriction results.

The contractile process ( including the initiation and termination of the action potential that causes it) of myocardial fibres is a complex process that involves sodium, calcium, and potassium as well as the intracellular organelles and structures within the myocardial cell.  It may be summarised by the following sequence of events that are illustrated below.
1) Sodium influx, via a sodium channel that either becomes activated (opens) in response to beta-1 receptor activation or changes in the membrane potential of the cell.

2) Calcium influx, via calcium channels that open in response to changes in cellular membrane potential.  (NOTE that different calcium channels with different characteristics are present in the SA/AV nodes and the ventricle illustrated here.)

3) The extracellular calcium diffuses to the sarcoplasmic reticulum (via the transverse tubules) where it acts as a primer to cause the release of additional calcium from the SR.

4) This calcium then interacts with the actin and myosin fibres to cause the contraction-coupling process (the muscle fibres contract).

5) The contraction is terminated upon the dissociation of calcium from the complex.  The calcium is then taken back up into the SR (by an ATP-dependent process) and stored for future use.

6) The extracellular calcium that entered via the calcium channel then dissociates from the SR and further release of SR calcium ceases.

7) (NOTE that the influx of extra-cellular sodium and calcium have now caused the membrane potential to be relatively more positive, near 0 mV.) Potassium channels have been activated, resulting in efflux of intracellular potassium ions, in an attempt to restore the resting membrane potential back to the preferred -90 mV.  The RMP has now returned to normal.  HOWEVER there are much higher levels of sodium and calcium and much lower levels of potassium within the cell that at the starting point.

8) The Na/K ATPase pump will now exchange the extracellular potassium for intracellular sodium, helping to restore the levels to those prior to the action potential and subsequent ion movement.

9) Additionally, a Na/Ca counter-transporter will exchange sodium for calcium, returning the calcium to outside the cell.

All of these ionic movements contribute to the action potential illustrated below.  Referring to the numbered sequence above, Sodium influx (1) causes depolarisation of the cell, Calcium influx (2) causes the plateau, potassium efflux (7) results in repolarisation of the cell, and the Na/K and Na/Ca exchange (8, 9) maintain the RMP.
 

Heart rate -- The heart normally beats 60 to 70 times/minute (70 is often the accepted average)

Stroke volume -- With each beat and left ventricular contraction, the heart will eject approximately 70 ml of blood into systemic circulation.

Cardiac Output is a function of both heart rate and stroke volume.  CO = (HR)(SV) = (70 beats/min)(70 ml/beat) = 4900 ml/min or an approximate CO of 5 L/min.

Preload -- RECALL that the contractility of a ventricle is a function of its muscle contraction AND the more stretched it is, the greater the contraction (more appropriately, in maths and physics terms, the greater the tension developed within the wall, the greater the contraction).  Therefore, the greater the stretch of the ventricle, the greater the preload (or predisposition to contract strongly).  Since the amount of blood within the ventricle greatly determines the degree of stretch AND since, in the normally functioning heart, the amount of blood in the ventricle is a function of the amount of blood being returned to the heart, preload may be roughly equated to venous return.

Afterload -- ALSO RECALL that in order for the heart to pump blood out to the periphery, it must generate a pressure that is greater than that encountered in the periphery (blood always flows from an area of higher pressure to an area of lower pressure).  The pressure that MUST be generated to exceed peripheral pressure is the AFTERLOAD.  In practical terms this is the aortic pressure.

Workload -- All of the above factors will contribute to the overall workload of the heart.  If preload increases, the heart will contract more strongly, ejecting more blood, decreasing the workload.  If afterload increases, it must generate greater pressure, increasing the workload.  The converse of each of these statements is also true.

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