Blood Pressure Regulation

SAMPLE PROBLEMS
 

	HR	SV	TPR	VR	CO	DP	SP	PP
ACh	D	I	D	D	D	D	I	I
EPI	I	I	D	I	I	?	I	I
NE	I	I	I	I	I	I	I	I

4 Factors Contibuting to Cardiac Output
• HR
• SV
• TPR
• VR

As HR increases,Filling Time Decreases!

Digitalis:  Decrease HR with no direct action on contractility or SV
But as filling time increases, EDV increases so SV increases according to…...

Venous Return:  see Fig 13.24
• Abdomino-Thorasic (Respiratory) Pump
• Skeletal Muscle Pump
• Ventricular Diastole
• Ventricular Systole

Skeletal Muscle Pump: Fig 13.23

Total Peripheral Resistance
• Increased TPR ---> Increased Arterial Pressure
• Increases work of heart and length of systole ( esp. isovolumetric phase)
• Decrease SV initially and briefly
• Also increases Arterial - Venous P
• increases amount of blood on venous side
• Increase VR and CO?
How do we resolve this apparent conflict/problem?
Depends upon ability of ventricles to increase SV

                     Consider exercise......
Response to Light Exercise: Fig 14.12

Blood Pressure
BP expressed in mm Hg

BP = CO x TPR

Pressure measured by baroreceptors
• Aortic arch
• Carotid sinus

VAGUS NERVE
• Parasympathetic fibers
• Baroreceptors from aortic arch
• Stretch receptors from lungs

Atrial Baroreceptors’ Responses:Fig 14.1

 

CHEMORECEPTORS

• P_O2 receptors
Carotid and aortic bodies
Brain stem - medulla
Sensitive to dissolved O₂
Only important at low  P_O2

Carbonic Anhydrase
CO₂ + H₂O <--> H₂CO₃ <--> H+ + HCO₃

Lungs                                   Kidneys
 

CHEMORECEPTORS:  CO₂ & pH
 AORTIC & CAROTID BODIES
MEDULLA
CO₂ + H₂O <--> H₂CO₃ <--> H⁺ + HCO₃^-

(AS CO₂ INCREASES,  PLASMA & CSF pH  DECREASES)
CO₂ DISSOLVES FROM PLASMA INTO CSF ACROSS BLOOD - BRAIN BARRIER
CO₂ + H₂O <--> H₂CO₃ <---> H⁺ + HCO₃^-
AS PLASMA CO₂ INCREASES, PLASMA pH DECREASES

CO₂  DISSOLVES INTO CSF, AND CSF pH DECREASES, STIMULATING MEDULLARY RECEPTORS

INPUTS:
• Baroreceptors (pns)
• Chemoreceptors (cns  &  pns)
• Atrial volume receptors
• Cerebral cortex
• Vasovagal syncope (fainting)
Corticohypothalamic response
Flight or fight response

Figure 14.2:  Whew !!

Medullary cardiovascular center
Vasomotor center
Pressor area
Cardioinhibitory center
Depressor area

Pressor or vasomotor center is spontaneously active and always slowed by depressor which is activated by baroreceptors

Decreased MAP:  Fig 14.3
Increased MAP:  Fig 14.3
Receptor-mediated response to hemorrhage: Fig 14.5
Receptor-mediated response to hemorrhage: Fig. 14.6

REFLEX RESPONSES
VASOVAGAL SYNCOPE:  FAINTING
CORTICOHYPOTHALAMIC DEFENSE REACTION:  FIGHT OR FLIGHT

RENAL CONTROL OF BLOOD VOLUME
Mammalian kidneys are designed to reabsorb Na+ and retain it in body fluids
increase Na+ reabsorption -->increase water reabsorption  -->increase blood volume --->
                RAISE  BP

ANTIDIURETIC HORMONE:(VASOPRESSIN or ADH)
• 9 amino acid peptide released from posterior pituitary
• released in response to:
    - elevated plasma 
    - lowered BP or lowered blood volume
    -(decreased atrial EDV and/ or decreased baroreceptor distention)

Normally ADH causes Na+ and water reabsorption by kidneys to increase blood volume and decrease plasma 
ADH released in response to low BP and not released when BP is high
 

ATRIAL NATRIURETIC PEPTIDE (ANP)
28 amino acid peptide hormone
released from atrial myocytes (muscle cells)
released in response to distention (high atrial EDV) due to high BP
INHIBITS  Na⁺ - K⁺ ATPase in kidney
THUS Na⁺ AND WATER ARE LOST IN URINE lowering blood volume

VOLUME RECEPTORS :  ATRIAL STRETCH RECEPTORS:
DECREASE  ADH
              And
  INCREASE ANP  (increase urine output and decrease blood volume)

ATRIAL STRETCH RECEPTORS RESPOND TO INCREASED BV BY:

RENIN -ANGIOTENSIN - ALDOSTERONE
LOW RENAL BLOOD FLOW
(< 20% OF CO)  ---> ACTIVATION OF  POTENT VASOCONSTRICTOR:
             ANGIOTENSIN

Things to Review and Know !
Table 14.1
Fig 14.7