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Lecture
Human Physiology
Monday, January 25, 2010
“CV X”
Cardiovascular Regulatory Mechanisms
•Types
Local (autoregulation)
Myogenic theory
•Resistance cells in arterioles are sensitive to pressure; can adjust resistance based
on resistance changes
Metabolic theory
•Adjusts vascular resistance as well
Humoral
Vasoconstrictors
•Epinephrine
•Norepinephrine
•Angiotensin II see Renal notes to review formation of AII
oHas direct & indirect effects
•Vasopressin (ADH)
oHigh concentration in blood following hemorrhage
Vasodilators
•Bradykinin: formed from alpha-2 globulin in plasma
•Histamine: derived from eosinophils & mast cells
•Adenosine: product of ATP metabolism
•Nitric oxide
Neural (mainly within the ANS) mostly control of blood pressure; function is to maintain a
normal arterial pressure
Cholinergic control
•Stimulates parasympathetic fibres to heart; causes decrease in heart and decrease
in blood pressure
Adrenergic control
•Stimulates sympathetic fibres to heart; release NE, which increase CO and BP
•Stimulates splanchnic nerve to adrenal medulla; release ACh, which increases CO
and BP
•Stimulates sympathetic vasoconstrictor fibres to peripheral vessels; releases NE,
which increases peripheral resistance and BP
•ANS control of arterial pressure
Mechanoreceptor (baroreceptor reflex pathway); respond to mechanical stretch; pathway
conveys info to CV centres in brainstem, which then feeds into efferent pathway to effector
organs (i.e. vascular muscle, heart, and sometimes glands)
Anatomic organization; see study guide
Sensors; can’t tell you absolute pressure – detect deviations
Baroreceptors located in aorta and carotid artery
CV centres in medulla (bilateral structures)
Vagal nucleus – parasympathetic output
Vasomotor centre – sympathetic output; solitary tract nucleus regulates this area
Medullary structures relatively autonomous (involuntary)
Any info received in solitary tract nucleus is also sent to higher centres of brain; weigh-in
more in more urgent situations
Areas connected to each other by interneurons
•Increase in BP . . .
Baroreceptors stimulated by stretch of BVs; increase their rate of firing, which increases output
to solitary tract nucleus
Activation of vagal centre; increases vagal traffic to heart; ACh release, and decrease in
HR and therefore BP
Activation of inhibitory neurons to vasomotor centre; decreased sympathetic outlofw to
heart and BVs (decreased HR, and decreased constriction of BVs)
•NO REAL activation of vasomotor centre; it functions by changing the amount of
inhibition (less inhibition = “activation”)
Response curve
Above 60mmHg in baroreceptors, firing rate starts to rise
•Decrease in BP. . .
Baroreceptors stretched less; frequency of firing is less
Reduced activation of vagal centre; less inhibition of heart rate, which increases BP
Reduced activation of inhibitory neurons; increased sympathetic outflow (increased HR
and therefore BP, and higher constriction and therefore BP)
•Mechanisms of regulation
Left side of table refers to cardiac output
Right side of table refers to total peripheral resistance
Emotional stress
Involvement of cortico-hypothalamic centres
Exercise
Function of volume receptors
Postural changes