Cardiovascular Physiology II

Objectives : this part helps the student to

- Identify the different determinants of blood pressure and its main
regulatory mechanisms.
- Describe the different mechanisms involved in regulation of diameter of
arterioles.

Cardiovascular centers :
a-Vasomotor center : these neurons mediate sympathetic discharge to blood vessels
and the heart. The cell bodies of these neurons are located in the ventrolateral nucleus
of the medulla oblongata and their axons descend in the lateral column of the spinal
cord. Stimulation of this center increases blood pressure by increasing HR and Sv and
by VC of blood vessels.
b- Cardioinhibitory center : It lies in the upper medial part of the medulla including
parts of dorsal motor nucleus of the vagus nerve, nucleus ambiuua and nucleus of
tractus solitarius. When stimulated, it increases vagal discharge to the heart
decreasing blood pressure and HR.
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c- Medullary sensory area : this area receives input from different parts of the body
and project to vasomotor center and cardioinhibitory center to regulate activities of
these centers together i.e. stimulation of one and inhibition of the other.

Arterial blood pressure

Definition : It is the lateral pressure exerted or produced by the blood on the arterial
walls.
Systolic blood pressure : it is the maximum pressure during systole. It is about
120mmHg.
Diastolic blood pressure : it is the minimum pressure during diastole . it is about 80
mmHg.
Pulse pressure : it is the difference between systolic and diastolic blood pressure.
Mean arterial blood pressure : It equals the diastolic blood pressure + 1/3 the pulse
pressure.
Importance of arterial blood pressure : It maintains the tissue perfusion,
responsible for capillary hydrostatic pressure, helps perfusion of parts of the body
above the level of the heart. In addition, the diastolic blood pressure is especially
important for maintenance of flow during diastole and is essential for coronary blood
flow.

Determinants of arterial blood pressure

APB = COP X TPR
aCOP = SV x HR So, increase cardiac output will increase ABP where increase
SV increases systolic blood pressure while increase in HR increases mainly
diastolic blood pressure.
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b-

TPR : increase in TPR (total peripheral resistance) increases the blood pressure
mainly diastolic blood pressure. The TPR depends on many factors The length
of the blood vessel (L) the viscosity of the blood, and the radius of the blood
vessel (r). The most important factor determining the resistance is the radius of
the blood vessel where TPR is inversely proportional to the r4.
cBlood volume : increase blood volume increases the blood pressure and vise
versa
dElasticity of the blood vessels : The elasticity of the aorta and big vessels
prevents marked increase of pressure during systole and marked drop of
pressure during diastole. Loss of elasticity of the arteries during atherosclerosis
converts elastic vessels into rigid tubes with high systolic and low diastolic
blood pressure and high pulse pressure.
Physiological factors affecting blood pressure :
- Age : the blood pressure increases with advance of age.
- Sex : The pressure is higher in males before menopause.
- After meals the blood pressure increases.
- During stress, exercise and emotions there is also increase in blood
pressure due to sympathetic stimulation.
- The gravity increases blood pressure below the level of the heart and
decreases it above the level of the heart.
- Environmental temperature : the hot weather decreases mainly diastolic
blood pressure due to cutaneous VD. While cold weather increases the
blood pressure due to cutaneous VC.

Regulation of the arterial blood pressure

I- Short term mechanisms : It includes ultrarapid and rapid mechanisms.
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- Ultrarapid mechanisms :
a- Arterial baroreflex : If arterial blood pressure increases it will stimulate the
baroreceptors in the carotid sinus and aortic arch where these receptors send afferent
impulses in vagus and glossopharyngeal nerves to the cardiovascular centers where
these impulses stimulate the cardioinhibitory center and inhibit the vasomotor center
so the HR, SV and TPR all are decreased and so the blood pressure decreases. The
opposite is true where decrease in blood pressure results in stimulation of vasomotor
center and inhibition of cardioinhibitory center with the end result of increased
arterial blood pressure.
This reflex is characterized by:
- They are very rapid reflexes.
- They prevent fall in the VR, COP and ABP when one sits or stands from the
lying down position.
- they act as buffer nerves because they prevent fluctuation of ABP.
- They respond to rapid and acute changes in ABP. With chronic changes
(gradual changes) in ABP these receptors adapt and reset to the new level of
blood pressure/.
b- Arterial chemoreceptors : These receptors are located in the carotid and
aortic bodies. They are stimulated by changes in arterial blood gases (oxygen , carbon
dioxide and hydrogen). When blood pressure decreases, the oxygen level in blood
perfusing these receptors is decreased and also the carbon dioioxide and hydrogern
level is increased. These changes stimulate the chemoreceptors which in turn
stimulate the cardiovascular center namely the vasomotor center to increase the blood
pressure.

c- CNS ischemic response : if blood pressure decreases, it will lead to ischemia

in the CNS, this will stimulate the vasomotor center to increase the blood pressure. It
is activated when the hypotension is marked below 60 mmhg.
- Rapid mechanisms : it includes release of two hormones the first is the
catecholamines and the second is the vasopressin and both increase the blood
pressure by causing VC and so increasing the TPR. And blood pressure.
II- Intermediate mechanisms : these include stress relaxation, capillary fluid shift
and rennin angiotensin mechanism.
III- Long term mechanisms :
a- It occurs through hormonal regulation affection renal function
a. Aldosterone hormone is secreted if blood pressure drops and causes
salt and water retention from the kidney increasing blood volume and
pressure
b. Atrial natriuretic peptide is secreted from right atrium if blood
pressure drops and causes salt and water execretion from kidney and
so blood volume and pressure drops

Regulation of diameter of arterioles

This regulation is achieved through two main mechanisms :
ILocal regulation
IISystemic regulation
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Local regulation of diameter of arterioles : it includes three mechanisms

autoregulation, local metabolites and endothelial vasoactive substances.
- Autoregulation : It is the ability of the tissue to keep or regulate its own
blood flow by regulating the diameter of its arterioles. Two theories are
proposed
i. myogenic theory : when blood pressure and blood flow increases
the smooth muscle in the wall of the arterioles constricts to
decrease blood flow.
ii. Metabolic theory : this theory states that increase metabolic
activity of an organ releases metabolites like hydrogen ions
carbon dioxide and this causes VD of arterioles to increase blood
flow and the opposite is true.
- Vasoactive metabolites these include hypoxia, decrease pH, increase
carbon dioxide, increase K ions , lactatic acid, histamine, adenosine,
increased temperature and potassium ions.
- Endothelial vasoactive substances :
a- Endothelium derived relaxing factor (EDRF or NO): it is a VD
substance released from endothelium
b- Endothelins : They are local VC substances released from
endothelium
systemic regulation of diameter of arterioles:
Hormonal regulation :
- circulating vasodilator substances include
i. -ANP (Atrial natruiretic peptide ) a peptide released from right
atrium
ii. Bradykinines
iii. Histamine.
iv. Acetylcholine.
- Circulating vasoconstrictor substances include circulating nor
epinephrine epinephrine, Angiotensin II, vasopressin and serotonin.
Nervous regulation of diameter of arterioles :
-Vasoconstrictor nerves include the sympathetic noradrenergic
-Vasodilator nerves include
- parasympathetic vasodilator nerves.All parasympathetic nerves contain
vasodilator nerves except the oculomotor nerve.
- sympathetic vasodilator cholinergic nerves to blood vessels of the
skeletal muscles and to the sweat glands