CVS REGULATION PART 2

SYSTEMIC BLOOD PRESSURE CONTROL

PRESENTER: DR WARAU WAWERU
FACILITATOR : DR. M DIN
 OUTLINE

 Neural control
 Humoral/ hormonal control
 Renal control
 Regulation of the cardiovascular: time frame
 Homeostatic consideration
 Cardiovascular system failure
NEURAL CONTROL
 Innervation of blood vessels
Primarily receives innervation from sympathetic
adrenergic fibers ---vasoconstriction via α adrenergic
- Abundant in the kidneys, intestines, spleen and skin

While vasodilation a result of activation of β2 by

epinephrine released from adrenals following symp
activation

*no parasympathetic division of the ANS innervating the

vasculature except on uterus, erectile tissue of the
reproductive organs, some facial & salivary blood vessels
Through sympathetic innervation
 Arterioles mainly regulate blood flow and pressure

 Venous capacitance regulate blood pooling in the

veins. Venoconstriction venous return
 Innervation of the Heart
The heart receives both sympathetic and
parasympathetic fibers.

NE released by the SNS  chronotropy

(HR), dromotropy (rate of transmission) and
inotropy (force of contraction)---via β1 receptors

Ach from the PNS (vagus nerve)  of above--- via

muscarinic receptors
 Nervous Control of CVS

Neural mechanisms involved in blood pressure control

include:
 Vasomotor center
 Sensory inputs- higher centers, direct stimulation
 Sensors – Baroreceptors and chemoreceptors
 Output – heart, blood vessels, adrenal medulla
 Sensors:
Baro/chemorec
eptors

Intergrating
Controlled center:  hypothalamus
variable: BP medulla, 
pons

cortex

Effector
Organs: heart, Output:
blood vessels, SNS/PNS
kidneys
Vasomotor center

Located bilateraly in
rostral ventrolateral
medulla (RVLM) and
1/3 of the pons

comprises of:
 Vasoconstrictor area
 Vasodilator area
 Sensory area
1.Vasoconstrictor area
-located on the anterolateral region of the upper
medulla aka rostral ventrolateral medulla (RVLM).

-Fibers from this area descend to the thoracolumbar

region (intermediolateral column) where they
secrete glutamate as their excitatory NT to activate
preganglionic symp neurons vasoconstriction 
HR, SV BP
2.Vasodilator area
-bilateral, anterolateral parts of the lower half of the
medulla. ---caudal ventrolateral medulla CVLM

- Send signals to the vasoconstrictor region to reduce

the neural output to the sympathetic nerves
3.Sensory Area

 Located bilaterally in the nucleus tract solitarious

(NTS) in the posterolateral portions of the medulla

 Receives signals from the vagus and

glossopharyngeal nerves

 Sends output signals to both vasoconstrictor and

vasodilator areas
Cardiac centers

Responsible for controlling HR and force of

contraction of the heart

 Cardioaccelerator- Sympathetic center –> Projects to

the SA, AV nodes & ventricular myocardium via the
cardiac sympathetic nerve.----NE

 Cardioinhibitory - Parasympathetic center –

>Projects to the SA and AV nodes via the CN X. ----
ACh
 Neural control

Neural influences to the vasomotor center

1. Input from higher centers- brainstem, insular
cortex, anterior temporal lobe, orbital areas of the
frontal cortex, limbic cortex
2. Direct stimulation
3. Sensory inputs- chemoreceptors and baroreceptors
1. Higher brain centers
 Hypothalamus – has both excitatory and inhibitory
effect in the VMC.
Posterolateral portion-->excitation; anterior
portion--> inhibitory
 Cerebral cortex (via hypothalamus)- excite and
inhibits VMC.
2. Direct Stimulation of VMC
-A drop in PO2 has been noted to depress the RVLM
----->vasodilation----> ↓BP

-Rise in arterial PCO2 and pH stimulates the RVLM ---

>vasoconstriction---> in tachycardia, increased cardiac
output, peripheral vasoconstriction---> increased BP

Note: direct peripheral effect of raised PCO2 leads to

vasodilation with concurrent vasoconstriction
elsewhere. Thus, slow rise in BP
3. Sensors

BARORECEPTORS / PRESSORECEPTORS
Stretch receptors found in
 the walls of blood vessels- carotid sinus, aortic
arch. High pressure arterial receptors
 Heart- RA (entrance of SVC and IVC), LA
(pulmonary veins, pulmonary circulation) also
known as cardiopulmonary receptors, are in the
low-pressure part of the circulation.
-Afferent fibers from
carotid sinus form a
branch of
glossopharyngeal
(through Hering’s
nerves) and fibers from
aortic arch form a
branch of vagus nerve.
 Baroreceptors respond much more to rapidly
changing or pulsatile pressures than to constant
pressures.

Threshold for triggering activity:-

 Carotid- 50mmHg; Max 200mmHg
 Aortic- >30mmHg
Cardiopulmonary (low pressure) baroreceptors

1. Atrial baroreceptors (type A and B)

A- discharge during atrial systole
B- discharge at peak atrial filling during venous return
-↓ by positive pressure breathing
Both types cause reflex vasodilation and reduced BP but
HR is rather than decreased

2. Ventricular baroreceptors
In the endocardial surfaces of the ventricles. Produces a
response similar to that of baroreceptor reflex.
 CHEMORECEPTORS

 Central
 Peripheral
 CHEMORECEPTORS

 Central
-In the medulla. Surface or within? Not known
In raised ICP-->reduced blood supply to RVLM-->
ischemia--> hypoxia, hypercapnia---> BP
*Cushing reflex

Rise in BP-->baroreceptors--> bradycardia

That’s why bradycardia in raised ICP is seen instead
of tachycardia
 Peripheral

-In carotid and aortic

bodies. Primarily respond
to hypoxia and secondarily
to hypercapnia and pH
changes

-Firing stimulates the

RVLM to initiate
vasoconstriction and
tachycardia in order to
raise BP
 ADRENAL MEDULLA

 The main secretions are the epinephrine,

norepinephrine and dopamine

 It serves as a sympathetic ganglion in which

postganglionic neurons have lost their axons and
become secretory cell

 These cells are stimulated by preganglionic neurons

resulting in release of NE and Epi stored in granules
Adrenal medulla..

 Both force and rate of

contraction of the heart via
β1 receptors

 Also increase myocardial

contractility

 On blood vessels, NE
- vasoconstriction via α1
 Epi – also causes
vasoconstriction expt in
skeletal muscle and liver ---
vasodilation via β2
Adrenal medulla..

 Apart from stimulation by the sympathetic fibers,

hypoxia also plays a role in stimulation of secretion
of catecholamines
HORMONAL CONTROL OF SYSTEMIC BP
 VASODILATORS

Kinins:

Two types:
• Bradykinin (nonapeptide)
• Kallidin (decapeptide) aka lysylbradykinin
• Kinins bind to type 2 bradykin receptors (BR2) 
vasodilation through prostacyclins, nitric oxide
(NO), endothelium-derived hyperpolarizing factor

• Kinins are primarily paracrines though small

amounts are found in circulation
 Natriuretic hormones
• Atrial Natriuretic Peptide (ANP):

Produced, stored and secreted into circulation by the

atrial myocytes in response to increased stretch of atria.

They promote loss of sodium and water  blood volume

and blood pressure drop.

↓ BP by causing:
• vasodilation of glomerular arterioles
• increased Na filtration at glomerulus
• decreased Na reabsorption at distal convuluted
tubules and cortical collecting duct
• inhibition of renin production
• inhibition of renal sympathetic nervous system
B-type or Brain Natriuretic Peptide (BNP):
• synthesized largely by the ventricles (as well as in the
brain where it was first identified)
• Similar physiological actions to ANP

C-type Natriuretic Peptide:

• Has paracrine activity (not secreted into circulation)
unlike ANP and BNP

• Produces vasodilatation (mechanism of action not

yet understood)
Vasoactive Intestinal Peptide/Polypeptide (VIP):

• Produced by a number of tissues (gut, pancreas,

suprachiasmatic nuclei of hypothalamus

• Binds to its receptor (VPAC2) expressed in smooth

muscles of blood vessels---vasodilation
 VASOCONSTRICTORS

 Vasopressin (ADH)
- Potent vasoconstrictor,
from posterior pituitary.

- Small amounts secreted

at a time hence plays
little in vasoconstriction.
Moreover, there's a
compensatory decrease
in CO producing little
change in BP
 Catecholamines

NE vasoconstrictor
Epinephrine vasoconstriction; mild vasodilator in
some tissues

Secreted from the post ganglionic sympathetic fibres

and adrenal medulla

In high concentrations, catecholamines preferentially

bind to α1-adrenergic receptors in vascular smooth
muscle causing vasoconstriction
 Angiotensin II

Renin  Angiotensinogen  Angiotensin I 

Angiotensin II
Angiotensin converting enzyme acting on
angiotensin I
Angiotensin II increases water intake and
stimulates aldosterone secretion from adrenal
cortex. This maintains ECF volume.

 Urotensin II- present in cardiac and vascular

tissue. Serve as markers in HTN and HF.
*research ongoing*
 RENAL MECHANISMS

Renal-body fluid system plays a major role in long

term regulation of BP- weeks, months

• Pressure Natriureris and Diuresis

• Renin-Angiotensin
• Aldosterone
• Erythropioetin secretion
 Pressure natriuresis; diuresis

An increase in arterial pressure by a few mmhg, can

lead to doubling of renal output of water i.e pressure
diuresis and salt i.e pressure natriuresis
 When H2O and salt intake and
output are equal, known as
equilibrium point

 As arterial pressure rises, urine

output increases causing
decrease in blood volume.

 Continues until pressure goes

back to equilibrium

 Conversely when pressure falls

below equilibrium point, intake
> output
 Increase renal artery pressure (RAP):
• Increase in GFR
• Increased peritubular capillary and interstitial pressure
• Reduction in number Na-H exchangers and N-K ATPase
activity at the proximal convoluted tubule leading:
increase Na excretion

-leading to net loss of water fall in CO, blood

volume- fall in BP
Renin-angiotensin System
 Erythropoietin secretion

 85% comes from the peritubular capillary beds of

kidneys and 15% comes from the hepatocytes of liver
 Other sources- spleen, salivary glands, brain, uterus
and oviducts
 Takes 2-3 days for new RBCs to appear
 EPO…
 Its secretion normally
triggered by hypoxia or
blood loss which causes
fall in renal perfusion.

 There are no preformed

stores

 It stimulates
erythropoiesis by
increasing the number
of progenitor cells in the
BM-rise in hematocrit
 Regulation of the CVS: Time Frame

ACUTE SHORT TERM LONG TERM

Neural (seconds) Hormonal (minutes) Renal
Baroreceptors (1 to 2 Circulatory reflexes
days)
CNS ischemic response: • Capillary fluid shift
• Due to fall in VMC • Venous volume
blood flow changes
• Last ditch response • Stress relaxation
• Massive symp outflow
 Homeostatic considerations
 EXERCISE
SHORT TERM
• HR and SV increases due to increase circulating
catecholamines, O2 demand and glucose requirements
CO  BP

• Vasodilation of blood vessels supplying myocardium, skeletal

muscles, lungs, liver and skin.

• Vasoconstriction of blood vessels supplying non-exercising

organs- visceral organs

• venous return--- preload--- stronger contraction-- CO

LONG TERM

• Ventricular hypertrophy --- SV

*Difference from pathological causes of hypertrophy :
-normal isovolumetric relaxation time & rate of LV filling
time
-no cavity enlargement or wall thinning

• ↓ resting HR, ↓ BP
• Widespread vascular remodelling and new capillary
formation
• Increased circulation blood volume
• Raised antioxidant levels
 ABNORMALITIES IN CONTROL

 Hypertension
 Hypotension
 CVS Failure
 Hypertensio
categories n Systolic Diastolic

Optimal <120 And <80

Normal 120-129 And/or 80-84

High normal 130-139 And/or 85-89

Grade 1 HTN 140-149 And/or 90-99

Grade 2 HTN 160-179 And/or 100-109

Grade 3 HTN >180 And/or >100

Isolated >140 and <90

systolic HTN

Adapted from the ESH/ISH guidelines)

NB: The class is determined by whichever of the readings is highest

KENYA NATIONAL CARDIOVASCULAR GUIDELINES 2018

 Hypotension

• BP lower than expected value for an individual in a

given environment

• Usually, BP < 90/<60 with symptoms

• Because arterial pressure is determined by cardiac

output, venous pressure and systemic vascular
resistance a reduction in any of these variables can
lead to hypotension.
Hypotension Sydromes:
• Pure Autonomic Failure (PAF): autonomic failure
• Idiopathic orthostatic hypotension -
• Vasovagal syncope
• Post-prandial hypotension

• Autoimmune autonomic neuropathy (AAN)

• Multiple System Atrophy (MSA)

 CVS FAILURE

• Occurs when CVS fails to:

• Supply O2 and nutrients
• Remove CO2 and toxic metabolites

• Cardiac or central circulatory collapse – heart and

great vessels affected

• Peripheral circulatory collapse – outlying arteries

and veins are affected
Causes of CVS failure are varied and multiple:
• Surgery
• Thrombosis
• Shock (cardiogenic, hypovolaemic, haemorrhagic,
septic, distributive)
• Heart disease (MI, CHF, ruptured/dissecting
aneurysms,
• Gangrene, organ failure
 References

 Ganong’s review of medical physiology

 Guyton and Hall textbook of medical physiology
 Physiology Elsevier by Linda Costanzo
 BRS Physiology 6th Edition
 Medscape
 THANK YOU