Blood Pressure Regulation Flashcards
what are the three major determinants of BP
- blood volume
- vascular resistance
- compliance
what is blood pressure and how does it change throughout the circulatory system
force exerted by the blood per unit area of the vessel wall
arteries: high pressure system
venous: low pressure system
what affects preload
vein compliance
blood volume
what is intrinsic regulation of blood flow
mechanisms used by the critical organs (heart, brain, kidney, spinal cord, working skeletal muscle) to maintain perfusion based on metabolic need
uses local mediators to maintain stable perfusion pressure to organs despite changes in systemic pressure
what are the short term BP regulatory mechanisms
- ANS regulation
- baroreceptor reflex
- chemoreceptor reflex
- arterial and pulmonary reflexes
what are the long term BP regulatory mechanisms
- RAAS system
- natriuretic peptides
how does ANS regulation of blood pressure work
vasomotor center (in medulla) sends signals to the heart and blood vessels via the spinal cord (SNS) or vagus nerve (PNS)
does SNS or PNS predominate BP signaling to heart and vasculature
sympathetic
parasympathetic predominates heart rate control
vasomotor tone
the continuous partial contraction of the vasculature that is maintained by the vasomotor center continuously transmitting signals
maintains baseline level of constriction (tone)
sympathetic nervous system receptor types and effects
a1/a2: arterioles and veins –> vasoconstriction
- arteriole vasoconstriction = decrease blood flow and increase SVR
- venous vasoconstriction = increase venous return/preload
B1: cardiomyocytes and conduction cells –> increase chrono/dromo/ino/lusitropy to increase CO
B2: coronary and skeletal arterioles –> vasodilation –> increase blood flow to coronary arteries and skeletal muscle
parasympathetic nervous system receptor types and effects
M2: SA and AV node, atria –> decrease chrono/dromotropy –> decrease CO and oppose SNS
baroreceptor reflex
negative feedback loop that relies almost exclusively on neural reflexes that control ANS
inc. BP causes stretch –> BR detect stretch –> increase firing to vasomotor center –> inc PNS and dec SNS –> vasodilation and decreased CO
where are baroreceptors located
carotid sinus
aortic arch
what afferent nerves do the baroreceptors in the carotid sinus use
hering’s nerve –> CN IX (glossopharyngeal)
what afferent nerves do the baroreceptors in the aortic arch use
aortic nerve –> CN X (vagus nerve)
what is the overall function of the baroreceptor reflex
to buffer acute changes in systemic BP associated with daily events
maintains a stable MAP despite acute changes
what two conditions decrease responsiveness of the body to baroreceptor signaling
- heart failure
- systemic hypertension
vago-vagal syncope
exaggerated baroreceptor reflex response in which a sudden change in posture/excitement can cause a drastic increase in PNS/decrease in SNS signaling
leads to rapid vasodilation and decreased HR –> sudden drop in BP –> syncope (fainting)
chemoreceptor reflex
responds to acute drops in pO2 and rises in pCO2 (when blood pressure drops below systolic 80 mmHg)
chemoreceptors signal to VM center –> increase in SNS signaling –> increase HR and vasoconstriction
components of the RAAS system that result in long term BP regulation
- ANG II
- aldosterone
- ADH
mechanism of RAAS system
JG apparatus sense decreases in BP or NaCl delivery –> JG cells release renin –> renin converts angiotensinogen to ANG I –> ACE converts ANG I to ANG II –> vasoconstriction + Na/H2O reabsorption + aldosterone + ADH secretion
what stimulates renin release
SNS stimulation
renal (and systemic) hypotension
decreased NaCl delivery to JG apparatus
what produces aldosterone and what are its effects
adrenal cortex
increase Na/H2O reabsorption
increase K excretion
overall increase in blood volume
what produces ADH and what are its effects
(vasopressin) posterior pituitary
increased water reabsorption
vasoconstriction
what are the effects of ANG II
vasoconstriction
aldosterone release
ADH release
direct stimulation of Na/H2O reabsorption
stimulates thirst
stimulates SNS
natriuretic peptides
hormones secreted by cardiomyocytes in response to wall stress of stretch
intrinsic mechanism in response to VOLUME overload
effect of natriuretic peptides
counteract diuretic hormones by causing vasodilation and Na/H2O excretion, and inhibiting renin release
BUT - body favors RAAS, so chromic RAAS and SNS stimulation overpowers natriuretic peptides
what can be used as a biomarker of heart disease
pro-BNP; synthesized by the ventricles
high levels indicates overproduction in response to a constitutive activation of RAAS during heart disease
