Non- nervous control of the heart

Control of heart rate

• The inherent autonomous discharge rate of the SA node is 100beats/min in the complete absence
of any nervous or hormonal influences on the SA node.

Local Control of the heart

Denotes mechanisms independent of nerves or hormones by which organs and tissues alter their own
arteriolar resistances, thereby self-regulating their blood flows.

This self-regulation is apparent in phenomena such as

a) Active hyperaemia,
b) Flow autoregulation
c) Reactive hyperaemia
d) Local response to injury

i. Active hyperaemia
 Most organs and tissues manifest an increased blood flow (hyperaemia) when
their metabolic activity is increased e.g. the blood flow to exercising skeletal
muscle increases e.g. the blood flow to exercising skeletal muscle increases in
direct proportion to the increased activity of the muscle.
 Active hyperaemia is the direct result of arteriolar dilation in the more active
organ or tissue.
ii. Flow autoregulation
 Autoregulation is a manifestation of local blood flow regulation. It is defined as
the intrinsic ability of an organ to maintain a constant blood flow despite changes
in perfusion pressure.
 When the flow of blood falls, arterial resistance (R) also falls as the resistance
vessels (the small arteries and arterioles) dilate.
 The oxygen dependence of tissue on blood flow is responsible for autoregulation in
organs with high oxygen consumption. Both the myocardium and the brain exhibit a high
degree of autoregulation, and in both of the organs blood flow is highly dependent on the
consumption of oxygen by the tissue.
iii. Reactive hyperaemia
 It is the transient increase in flow of blood in an organ that occurs following a brief
period of ischemia (arterial occlusion) or arterial blockage. In this example, the flow of
blood goes to zero during the arterial occlusion.
 Reactive hyperemia is the term used to describe the transient increase in flow rate above
the control level which follows an interval of arterial occlusion.
  It ensures that, post-occlusion, all cells will receive enough oxygen rapidly, and any dead
cells and metabolic wastes will be swiftly flushed out from the area to reduce continued
damage.
iv. Local response to injury
 Myocardial infarction is associated with an inflammatory reaction, which is the
prerequisite for the healing and the formation of scar.
 When the tissue is first injured, small blood vessels in the damaged area constrict
momentarily, the process called vasoconstriction. After this transient event, which is
believed to be of little importance to the inflammatory response, the blood vessels dilate
(vasodilation), increasing blood flow into the injured area.
 Coronary artery occlusion critically reduces blood flow to the portion of the myocardium
subserved, markedly impairing the energy metabolism.
 These abnormalities are not attended by lethal injury and the ischemic myocardium
ultimately recovers.
 This transient functional abnormality (the stunned myocardium) is related to the reactive
oxygen formation, but shows little if any evidence of an inflammatory reaction.
 However, ischemia of significant duration to induce infarction does result in an
inflammatory response, this response is both accelerated and augmented if the ischemic
tissue is reperfused.
Hormones

 Epinephrine, like norepinephrine released from sympathetic neurons, can bind to

α-adrenergic receptors on arteriolar smooth muscle and cause vasoconstriction.
 However, because many arteriolar smooth muscle cells possess the β2 subtype of adrenergic
receptors as well as α-adrenergic receptors, and the binding of epinephrine to β2 receptors
causes the muscle cells to relax rather than contract .
 Another hormone important for arteriolar control is angiotensin II, which constricts most
arterioles.
 Another hormone that causes arteriolar constriction is Antdiuretic Hormone (ADH) also
known as vasopressin, which is released into the blood by the posterior pituitary in response to
a decrease in blood pressure.
 Atrial natriuretic peptide is a hormone secreted by the cardiac atria—is a potent vasodilator.
 Atrial natriuretic peptide does influence blood pressure by regulating Na + balance and blood
volume.

References

Barret, K.E, Barman, S.M, Boitano, S, Brooks, H.L. Ganong’s Review of Medical Physiology,
25th Edition. McGraw Hill Education, (2016), New York, USA.
Hall,J.E, Guyton and Hall Textbook of Medical Phyiology 13th Edition. Elsevier,
(2016), Philadelphia, USA.

Silverthorn, D.U, Human Physiology An Integrated Approach, 5th Edition.

Pearson Benjamin Cummings, (2010), San Francisco, USA.

Waugh, A .Grant, A. Rolls & Wilson Anatomy & Physiology in Health and Illness,
12th Edition. Churchill Livingstone Elsevier, (2014), New York, USA.