HARARE POLYTECHNIC

SCIENCE TECHNOLOGY DIVISION

COVER SHEET

FIRST NAME(S): VALENTINE . SURNAME: MHUTE .

COURSE: ND1 PHARMACY DATE: 23-11-2020 .

NAME OF LECTURER: MR P MOYO .

SUBJECT: HUMAN PHYSIOLOGY .

ASSIGNMENT/PRACTICAL: ASSIGNMENT 2 .

MARK: MODERATE MARK: .

COMMENTS:

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LECTURER’S SIGNATURE: DATE: .

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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.

1. Local Control of the heart

It indicates the mechanisms that are independent of the nerves or hormones by which the
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, then the blood flow to exercising skeletal
muscle also increases. For example, the flow of blood to the exercising skeletal
muscle increases in direct proportion to the increased activity of the muscle.
 Active hyperaemia arises because of the dilation arteriolar in the more active
organs or tissues.

ii. Flow autoregulation

 Autoregulation is a manifestation of the local flow of blood regulation. It is
defined as the essential ability of an organ to maintain a constant flow of blood
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 inflow 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 arterial occlusion.
 Reactive hyperemia is a name used to portray 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

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 reduce continued damage.

iv. Local response to injury

 Myocardial infarction is associated with an inflammatory reaction, which is
necessary for the healing and the formation of a scar.
 If the tissues are injured first, the small blood vessels in the damaged area
constrict momentarily. This process called vasoconstriction. After this temporary
event, which is believed to be of little essentialness to the inflammatory response
of the tissues, the blood vessels dilate (vasodilation), increasing the flow of blood
into the injured area.
 Coronary artery occlusion critically decreases the flow of blood 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.
 However, ischemia of significant duration to induce infarction does result in an
inflammatory response by body tissues, this inflammatory response is both
accelerated and augmented if the ischemic tissue is reperfused.
Hormonal Control of the Heart

 Epinephrine, like the norepinephrine released from the sympathetic neurons of the
sympathetic nervous system, can bind to the α-adrenergic receptors on an arteriolar
smooth muscle and cause the muscle to constrict (vasoconstriction).
 However, because many of the arteriolar smooth muscle cells possess the β2 subtype of
the adrenergic receptors, as well as α-adrenergic receptors and the binding of the
epinephrine hormone to the β2 receptors causes the relaxation of the muscle cells rather
than contract.
 Another crucial hormone for the control of arteriolar is angiotensin II, which constricts
most of the arterioles.
 Another hormone that causes arteriolar constriction is Antidiuretic Hormone (ADH) also
known as vasopressin, which is released into the blood by the posterior pituitary in
response to a decrease in blood pressure.
 The atrial natriuretic peptide is a hormone secreted by the cardiac atria—is a potent
vasodilator.
 Atrial natriuretic peptide does have an effect on the pressure of blood by regulating Na+
balance and blood volume.

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References

Barret, K.E, Barman, S.M, Boitano, S, Brooks, H.L. (2016). Ganong’s Review
of Medical Physiology, 25th Edition. McGraw Hill Education, New York, USA.
Hall,J.E,(2016), Guyton and Hall Textbook of Medical Phyiology 13th Edition.
Elsevier, Philadelphia, USA.
Sherwood, L,(2010). Human Physiology From Cells to Systems, 7th Edition.
Brooks Cole Cengage Learning, West Virginia, USA.
Silverthorn, D.U,(2010). Human Physiology An Integrated Approach, 5th Edition.
Pearson Benjamin Cummings, San Francisco, USA.
Waugh, A .Grant, A. (2014). Rolls & Wilson Anatomy & Physiology
in Health and Illness, 12th Edition. Churchill Livingstone Elsevier,
New York, USA.