CHAPTER III: ARTERIAL PRESSURE
CONTROL
Asst. Prof. Dr. Emre Hamurtekin
EMU Faculty of Pharmacy
• CVS system includes two distinct pathways for monitoring and
maintaining arterial pressure:
 Baroreceptor Reflex (fast activating)
 Sensors – Integrator – Effector mechanisms
 Changes in blood volume by renal function (slow activating)
• Sensors:
I.
II.
III.
High-pressure arterial baroreceptors
Low-pressure cardiopulmonary receptors
Chemoreceptors
• Clusters of sensory nerve endings
• Aortic baroreceptors and carotid baroreceptors are the
primary means of detecting changes in MAP.
• They respond to arterial wall stretch.
• Aortic baroreceptors
aortic nerve
vagus nerve
• Carotid sinus
sinus nerve
glossopharyngeal nerve
• The sensory nerves respond to stretching of the arterial wall
because of the increasing MAP with graded receptor potentials.
• Sensory nerve endings embedded in the walls of the
vena cavae
pulmonary artery and vein
atria
low-pressure regions
• They provide CNS (by vagal nerve) with information about the
«fullness» of the vascular system.
• Their principal role is in modulating renal function.
• They also have a role in maintaining MAP.
• Monitor local metabolite levels which reflect the pressure and
flow.
• Highly vascularized glomus cell clusters
• Located in aortic arch (aortic bodies) and carotid sinus (carotid
bodies).
• PO2 ˂ 60 mm Hg
• PCO2 ˃ 40 mm Hg
• PH ˂ 7.4
activation
• Principally involved in respiratory control but also reflect low
perfusion pressures.
• Medulla oblangata
Vasomotor center
(vasoconstriction)
Cardioacceloratory center
(positive chronotropy and
inotropy)
Cardioinhibitory center
(negative chronotropy)
CARDIOVASCULAR CONTROL CENTER
INPUT
IMPULSE
Low / High MAP
OUTPUT
-
Cardioinhibitory
-
Cardioacceleratory
HR
HR
INOTROPY
Inhibitory interneuron
Inhibitory interneuron
Vasomotor
PRELOAD
SVR
MAP = CO x SVR
• Control centers adjust both CO and SVR.
• Control is exerted by simple feed back loops.
When MAP falls, baroreceptor reflex starts and:
1. SVR increases
2. Venoconstriction
3. LV preload increases
4. Inotropy increases
5. HR increases
6. CO increases
7. SNS activation causes the adrenal glands secrete epinephrine
• This is responsible for
circulating blood volume and
Na regulation.
• These pathways converge on
the kidney.
Water output
Water intake
REGULATIONS
Sodium output
Sodium intake
• Water output is controlled by
ADH (antidiuretic hormone,
vasopressin, AVP).
1. ADH stimulates water reabsorption by the renal collecting
tubules.
2. Increase in SVR by constricting arterial vessels.
REGULATION of ADH:
- Osmoreceptors: When osmolarity exceeds 280 mOsm/kg, ADH
release is stimulated
- Baroreceptors: Decrease in circulating blood volume is detected
by cardiopulmanary and arterial baroreceptors and ADH
release is stimulated.
- Angiotensin-II: Angiotensin-II stimulates hypothalamus to release
ADH.
• Decrease in blood volume
• Decrease in arterial pressure
Triggers thirst and drink water
Macula densa
RENIN
JUXTAGLOMERULAR APPARATUS
1. Vasoconstriction.
2. Stimulates ADH release
3. Stimulates thirst and salt
apetite.
4. Promotes aldosterone
release from adrenal
cortex.
---------------------------------• Aldosterone targets the
renal collecting tubule
epithelium.
• Increases Na and water
reabsorption.
• Salt craving triggers a need to ingest NaCl.
• Salt apetite is stimulated by aldosterone and Ang-II.